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Drogenabhängige sind gegen kostenloses Heroin“, berichtet Politiken. Wie die dänische Tageszeitung erklärt, können sich Süchtige seit zehn Monaten in öffentlichen Hilfseinrichtungen kostenlos rezeptpflichtige Heroin-Dosen verabreichen lassen. Es handelt sich um reines Heroin, dass ohne jede strafrechtliche Verfolgung konsumiert werden kann. Dennoch haben nur 80 Menschen dieses Angebot in Anspruch genommen, an das ebenfalls eine Behandlung gebunden ist. Insgesamt verfügen die Einrichtungen über 300 Plätze. „Die Behandlung schränkt den Patienten sehr ein, wird streng überwacht und kontrolliert“, erklärt der leitende Sozialmediziner der dänischen Hauptstadt. Die Drogenabhängigen müssen ein oder zwei Mal täglich in die Einrichtung kommen und jede einzelne Dosis muss unter medizinischer Aufsicht eingenommen werden. „Wenn die Junkies das vom Staat bezahlte Heroin ablehnen, ist klar, dass das Programm überarbeitet werden muss“ und die betroffenen Personen vielmehr angehört werden müssen, meint Politiken.
Bonn/Rheinbach. Dass in vielen Gefängnissen nicht nur Handys und Alkohol, sondern auch Drogen unter den Gefangenen gehandelt werden, ist ein offenes Geheimnis. In der Justizvollzugsanstalt (JVA) Rheinbach sollen sich jetzt sogar zwei Beamte mit sechs Gefangenen und zwei externen Dealern zusammengetan haben, um den Handel mit Heroin und Cannabis professionell zu organisieren.
Foto: Saxler-Schmidt
Wie Oberstaatsanwalt Robin Faßbender am Mittwoch mitteilte, wurden die zehn Männer im Alter zwischen 27 und 52 Jahren jetzt wegen bandenmäßigen Drogenhandels sowie Bestechlichkeit und Bestechung im besonders schweren Fall angeklagt. Voraussichtlich müssen sie sich demnächst vor der 3. Großen Strafkammer des Bonner Landgerichts verantworten.
„Ein derartiger Fall ist im hiesigen Bereich noch nicht bekannt geworden“, so Faßbender zu der Dimension des Drogenhandels hinter Gittern. Bei 13 Taten, die in den Augen der Staatsanwaltschaft nachgewiesen werden können, sollen 635 Gramm Heroin und 800 Gramm Cannabis in das Gefängnis eingeschleust worden sein.
Der Verkauf der Drogen brachte anscheinend mehr als 100 000 Euro ein. Die Initiative soll im März 2008 von zwei Insassen der JVA ausgegangen sein: Offenbar wussten sie, dass ein 52 Jahre alter Bediensteter in finanziellen Schwierigkeiten steckte.
Der Vollzugsbeamte ließ sich schließlich laut Anklage auf den Plan der Männer ein: Von zwei Dealern bekam er die in Päckchen verpackten Drogen nach Hause in seinen Briefkasten geliefert, so der Oberstaatsanwalt. Anschließend soll er die Päckchen in die JVA geschleust haben.
Dort hatten die beteiligten Gefangenen, die allesamt mehrjährige Haftstrafen absitzen, anscheinend ein regelrechtes Handelsnetz aufgebaut: Neben den Drogen sollen auch eingeschleuste Waren wie Mobiltelefone und Sonnenbrillen an die Mithäftlinge verkauft worden sein.
Wenn Gefangene Bestellungen aufgaben, sollen sich die Bandenmitglieder bei einem mitangeklagten 36 Jahre alten Beamten – der Einblick in die Gefangenenkonten hatte – erst einmal über deren finanzielle Verhältnisse Klarheit verschafft haben.
Doch im November 2008 bekamen die Ermittler Wind von dem Treiben: Ein 43 Jahre alter Häftling, der an den Bestellungen und dem Verkauf der Drogen beteiligt gewesen sein soll, packte aus. Es folgten verdeckte Ermittlungen, bei denen vor allem etliche Handys überwacht wurden.
Im März 2009 schlugen die Fahnder der Ermittlungsgruppe „Briefkasten“ dann zu: Sie durchsuchten unter anderem bei dem 52-Jährigen und nahmen den Vollzugsbeamten in Untersuchungshaft. Nach fünf Monaten wurde er gegen Auflagen wieder auf freien Fuß gesetzt.
Dass erst jetzt Anklage erhoben wurde, lag laut Faßbender an den langwierigen Ermittlungen – insgesamt wurden Verfahren gegen mehr als 100 Personen eingeleitet – und der sich nur nach und nach entwickelnden Aussagebereitschaft der inzwischen teilgeständigen Angeklagten. Das Fall wird in Kürze am Bonner Landgericht verhandelt.
Artikel vom 10.03.2011 http://www.general-anzeiger-bonn.de/index.php?k=loka&itemid=10001&detailid=860047
DOCTORS are writing thousands of suspect prescriptions for a pharmaceutical variation of heroin, much of it destined for the black market, forcing the federal government to investigate the actions of 50 medical practitioners.
More than 580,000 taxpayer-funded scripts were approved in NSW in the past two years for OxyContin and similar opiate painkillers, such as OxyNorm and MS-Contin, dubbed “hillbilly heroin“.
For every $34 script of OxyContin, users are obtaining a box of 20, 80 milligram tablets. Each tablet can then sell on the black market for as much as $50. With further subsidies to pensioners, the box can be bought for as little as $6 – and its contents might be sold on the street for $1000.
While the medication has revolutionised care for chronic pain sufferers, it is leaking out of the health system to such an extent that police and health experts warn it could soon surpass street heroin and ice as the needle addict’s drug of choice.
The prescription opioids are obtained unlawfully by dealers and addicts who “doctor shop“ for multiple prescriptions. One patient visited 46 doctors in three months and obtained 119 scripts, primarily for OxyContin, the government has confirmed.
Sydney doctor Alan Saunders, who has been targeted by doctor shoppers, warned: „It’s not just OxyContin – it’s valium and all the other drugs. The government is subsidising the drug trade.“
Pharmacists say they are confronted with stolen and fake scripts, while legitimate pain sufferers are obtaining the drug and then selling it.
The government acknowledges the problem. Federal Minister for Human Services Tanya Plibersek confirmed to The Sun-Herald that Medicare had identified 50 doctors for “unusually high levels of prescription writing for drugs such as OxyContin and OxyNorm“.
„The misuse of prescription narcotics is a growing problem which destroys lives and tears communities apart. Doctors suspected of making these drugs available to patients who do not require them for clinical purposes will be put on notice.“
With a slow-release formula, OxyContin capsules are designed to work through the day. Illicit users, however, discard the other binding agents and extract the drug in its purest form so, when injected, it delivers an instant hit.
According to new state government statistics released to The Sun-Herald, more than $557 million worth of illegal drugs were seized in the state last year – more than double the street value of the previous year’s tally of $260 million. The haul included $185.2 million worth of cannabis, $126 million of cocaine, $195 million of amphetamines and $28 million of MDMA/ecstasy. NSW Police Minister Michael Daley said the figures showed police were doing “a fantastic job keeping our streets safe“, adding: “It’s millions of doses of deadly substances that have been kept out of the veins of would-be drug users.“
Significantly, NSW police also seized more than $25 million worth of heroin. At the same time, a taxpayer-funded version of the drug is infiltrating the black market. The commander of the NSW drug squad, Nick Bingham, said: “We’re talking pharmaceutical-grade heroin. It’s highly sought after in the drug-using community and, unfortunately, it is finding its way [onto the streets]. To be honest, police don’t particularly want to have to target prescription opiates when there are other important things to tackle, such as organised crime.“
Inspector Bingham is part of the recently formed National Pharmaceutical Misuse Strategy Committee and said prescription opiates were “high on the agenda … One of the discussion points is educating doctors in regards to prescriptions … there needs to be tighter scrutiny.“ The director of the Alcohol and Drug Service at St Vincent’s Hospital, Alex Wodak, agrees major reforms are needed to improve the way opiates are prescribed by the medical profession: “The process needs to be far more discriminating, more realistic, more careful.
“GPs do the bulk of this work. They’re under tremendous pressure and could do with better assistance from the whole system, whether it be from medicine doctors, psychiatrists, pain doctors or better guidelines tailored to them.“
Dr Wodak also referred to the “long overdue“ national real-time database which, if implemented, could alert authorities when “runners“ try to use multiple scripts at different chemists, at different locations.
“The Commonwealth seems interested in trying to get all the states to adopt a similar live system,“ he said. “If we are serious about this issue, we have to form a national response.“
But Richard Mattick, from the National Drug and Alcohol Research Centre, fears a crackdown could hit genuine pain sufferers.
“Let’s not forget these medications are terribly important to the community,“ he said. “If you have a loved one affected by cancer or serious pain, you want them to receive the best possible care and these medications are much better, much safer than anything previously available. The community is better served and, in a way, that has allowed prescribing to be more generous.
“The danger here is that we see the bad side but don’t balance that against the need.“
Gideon Warhaft, of the NSW Users & AIDS Association, argues: “There will always be people who inject drugs and there will always be people with narcotics dependencies. The positive advantage with OxyContin is that users know exactly what they’re getting, whereas with heroin, they don’t. Many now prefer OxyContin because it’s clean and it’s safer.“
„Better than heroin“ … Stephen buys Oxycontin from people who are terminally ill. Photo: Jacky Ghossein
FORMER heroin user Stephen* has been using Oxycontin for six years but has a better alternative than doctor shopping. He buys the drug from terminally ill people who use the funds as a legacy for their families.
“I got introduced to Oxycontin by a sick friend who was being prescribed it. They were receiving roughly 30 per cent more than they needed so I took it off their hands.
“There are a lot of terminally ill people out there who get so much of this stuff, they’re selling it and making a fortune. It’s their legacy, for their kids … it’s a far better option than doctor shopping, taking risks and ending up in jail. They’re helping you and you feel as though you’re helping them.“
He said the Oxycontin rush wasn’t as intense as heroin and it wore off more quickly but the feeling was “extremely similar“ to heroin and many users preferred it.
“Heroin can be dangerous, particularly if you don’t know where it’s come from … I have overdosed twice. But with Oxycontin, you know exactly what dose you’re getting and at $30-$40 for an 80 milligram tablet, it’s far better value for money.“
He said if politicians came down on Oxycontin, users would “revert … to heroin – which can mean stealing, armed robberies and doing absolutely anything to fund it“.
source: http://www.smh.com.au/nsw/legal-heroin-sold-to-addicts-20110305-1bipy.html
More young people are becoming addicted to heroin in Burma’s northernmost Kachin state as authorities fail to clamp down on dealers, sources in several towns have warned.
Males between the ages of 17 and 40 were among the most affected,s aid a resident of Mogaung town, which lies just west of the Kachin capital, Myitkyina. Other towns suffering rising rates of addiction were Mohnyin, Myitkyina and Hpakant, he added.
“The kids are so ruined,” the man said. “Everyone, from students aged around 18 to even farmers, are addicted to heroin. They were only trying it out at the beginning but now are addicted.”
He continued that most addicts were injecting the drug, a cheaper method despite the health risks. One intra-venous hit, he said, cost around 1000 kyat ($US1), while smoking through a pipe costs up to 4000 kyat ($US4.50).
A group of heroin dealers were reportedly arrested last month in Mohnyin by the government’s Anti-Drugs Task Force (ADTF) but later released on bail. The man said they had quickly got back to dealing.
Burma
Assertions by the Burmese government that it is stamping out the country’s lucrative drugs trade have been widely doubted: the US released a report last week saying that Burma had “demonstrably failed” to halt the trade of heroin and its derivative, opium, whilst statistics showed that in-country production of methamphetamine continues to rise.
The report was followed by an announcement in the state-run New Light of Myanmar newspaper that 15,021 acres of poppy fields were destroyed in 2010-2011, 411 of which were in Kachin state. Regardless, however, criticism continues to abound.
“The government is the main culprit for this,” said the Mogaung resident. “The government is the first to blame and the dealers the second. They are openly selling drugs on a tray.”
He claimed that dealers paid monthly bribes of up to 400,000 kyat ($US450) to government officials, including the ANTF.
Two years ago the Kachin News Group released an alarming report claiming that a significant number of students at the once prestigious Myitkyina University in Kachin state had fallen victim to drug addiction, notably heroin, with dealers initially luring students in with free samples.
Until the late 1990s and the explosion in Afghan heroin, Burma had held the distinction of being the world’s leading source of the narcotic, with the ethnic United Wa State Army producing hundreds of thousands of tonnes each year.
A report released last year by the Thailand-based Shan Drug Watch claimed that junta-backed militias had taken over ethnic armies as Burma’s main drugs’ producers, with the product finding its way to neighbouring Thailand and China.
source:http://www.eurasiareview.com/world-news/asia/burma-heroin-use-up-as-supply-goes-unchecked-08032011/
There has been a dramatic decrease in the amount of heroin in the UK, BBC News has learned.
The Serious Organised Crime Agency claimed the drop was due to supply routes being cut off and said the street price of the drug had doubled.
Europe’s biggest drug testing company, Concateno, said the number of addicts testing positively for heroin had halved in the past six months.
However, it warned that suppliers were diluting heroin with other drugs.
If heroin purity returned to normal levels, addicts would face an increased risk of overdose.
There are an estimated 300,000 users of heroin, which comes mainly from Afghanistan and Pakistan, in the UK.
Concateno takes swabs from anyone on a court testing order or in drug treatment for heroin.
Its figures show positive tests occurring in up to 48% of cases over recent years, but last December the rate fell to 22%.
The suggestion of an interruption in the supply is backed up by police reports of shortages in several places in the UK.
Officers from the Serious Organised Crime Agency (Soca) point to both the efforts of law enforcement agencies and environmental factors such as the floods in Pakistan.
And they say exaggerated perceptions among traffickers of a poppy blight may have led dealers to hold their supplies back and create higher prices on the street.
Relationships between Soca and the Turkish police are also said to be strengthening, leading to pressure on what has been a key supply route.
The drug is now said to command £40,000 a kilo – double the price of last year.
Posted by the BBC
Schlafmohn, aus dem natürlich Opioide gewonnen werden
Schmerzpatienten müssen geduldig sein. Oft vergehen leidvolle Jahre mit einer Odyssee von Arzt zu Arzt, bis sie endlich eine angemessene Behandlung erfahren. Aber auch die Geduld von Schmerztherapeuten wird strapaziert. Nachdem Pioniere wie Thomas Flöter in Frankfurt am Main und Dietrich Jungck in Hamburg vor fast dreißig Jahren die ersten kassenärztlichen Praxen für Schmerztherapie eröffnet hatten, war es noch ein steiniger Weg zu der Einsicht in der Ärzteschaft, dass Schmerz als eigenständige Krankheit auftreten kann.
Nun sehen Schmerztherapeuten neues Unheil heraufziehen. Anlass ist eine im vergangenen Herbst vorgelegte Leitlinie mit dem Kürzel „Lonts“, in der die Langzeit-Anwendung von Opioiden bei nicht tumorbedingten Schmerzen in Frage gestellt wird. „Über drei Monate hinausgehende Daueranwendungen opioidhaltiger Analgetika haben keine nachgewiesenen anhaltenden Schmerzlinderungen erbracht“, lautet eine der Schlussfolgerungen. Auf dem Deutschen Schmerz- und Palliativtag vergangene Woche in Frankfurt am Main sorgte dieses Papier für Empörung. Man ging mit ihm hart ins Gericht.
Schlafmohn, aus dem natürlich Opioide gewonnen werden
29. März 2010
Schmerzpatienten müssen geduldig sein. Oft vergehen leidvolle Jahre mit einer Odyssee von Arzt zu Arzt, bis sie endlich eine angemessene Behandlung erfahren. Aber auch die Geduld von Schmerztherapeuten wird strapaziert. Nachdem Pioniere wie Thomas Flöter in Frankfurt am Main und Dietrich Jungck in Hamburg vor fast dreißig Jahren die ersten kassenärztlichen Praxen für Schmerztherapie eröffnet hatten, war es noch ein steiniger Weg zu der Einsicht in der Ärzteschaft, dass Schmerz als eigenständige Krankheit auftreten kann.
Nun sehen Schmerztherapeuten neues Unheil heraufziehen. Anlass ist eine im vergangenen Herbst vorgelegte Leitlinie mit dem Kürzel „Lonts“, in der die Langzeit-Anwendung von Opioiden bei nicht tumorbedingten Schmerzen in Frage gestellt wird. „Über drei Monate hinausgehende Daueranwendungen opioidhaltiger Analgetika haben keine nachgewiesenen anhaltenden Schmerzlinderungen erbracht“, lautet eine der Schlussfolgerungen. Auf dem Deutschen Schmerz- und Palliativtag vergangene Woche in Frankfurt am Main sorgte dieses Papier für Empörung. Man ging mit ihm hart ins Gericht.
Vor gar nicht langer Zeit herrschte unter Ärzten noch die Ansicht vor, Schmerzen seien stets eine Begleiterscheinung von „echten“ Erkrankungen. Die Schmerzbekämpfung galt gewissermaßen als Nebentätigkeit des jeweiligen Facharztes. Rückenschmerzen etwa fielen klar in die Zuständigkeit des Orthopäden. Besondere Kenntnisse schienen nicht nötig zu sein: bei leichten Beschwerden ein leichtes Mittel wie Paracetamol, bei starken Leiden notfalls ein Opioid.
Unermüdlich haben Ärzte, die über Erfahrung in spezieller Schmerztherapie verfügen, mit wissenschaftlicher Unterstützung gegen dieses Schubladendenken angekämpft – mit Erfolg. Inzwischen orientieren sich informierte Therapeuten nicht mehr nur an der Stärke des Schmerzes, sondern vor allem an den von Patient zu Patient oft recht unterschiedlichen Mechanismen. So kann es angebracht sein, das Stufenschema auf den Kopf zu stellen und auch bei nicht tumorbedingten Schmerzen gleich ein Opioid anzuwenden, damit die Beschwerden nicht chronisch werden. Chronischer Schmerz kann sogar Hirnstrukturen verändern und ist schwer auszulöschen. Soeben ist in den „Proceedings“ der amerikanischen Nationalen Akademie der Wissenschaften (doi: 10.1073/pnas.1001504107) der Bericht einer finnischen Forschergruppe um Sanna Malinen erschienen, dem zufolge chronischer Schmerz auch bei ruhenden Patienten mit einem auffälligen Aktivitätsmuster im Gehirn einhergeht.
Ungezählte Patienten mit chronischen Schmerzen haben von der dauerhaften Opioidanwendung schon profitiert. Diesen Erfolg sehen viele Therapeuten durch die neue Leitlinie gefährdet, und entsprechend harsch fiel die Kritik aus. Der Psychologe Hardo Sorgatz von der Technischen Universität Darmstadt, unter dessen Leitung „Lonts“ im Auftrag der Deutschen Gesellschaft zum Studium des Schmerzes erarbeitet wurde, versuchte in Frankfurt einen verbalen Präventivschlag zur Verteidigung der Leitlinie. Diese genüge strengsten methodischen Kriterien und beruhe ausschließlich auf den Ergebnissen der wissenschaftlich aussagekräftigsten Studien. Doch Michael Überall vom Nürnberger Institut für Qualitätssicherung in Schmerztherapie und Palliativmedizin förderte hinter der Glanzfassade des Wissenschaftsgebäudes etliche Risse zutage. Er attestierte „massive methodische Schwächen bei der Analyse von wissenschaftlichen Studien“, die „zu falschen Schlussfolgerungen für die Langzeit-Therapie mit Opioiden“ führten.
Aufwendige Studien zur Wirkung von Opioiden und anderen Schmerzmitteln stammen häufig aus den Zulassungsverfahren für neue Medikamente. Diese erstrecken sich aber kaum über mehr als drei Monate, so dass man ihnen tatsächlich nichts über eine längere Anwendungsdauer entnehmen kann. Für den Präsidenten der Deutschen Gesellschaft für Schmerztherapie, Gerhard Müller-Schwefe aus Göppingen, steht der Nutzen für viele Patienten gleichwohl außer Frage. Nur lässt er sich schwer wissenschaftlich dokumentieren, denn dazu müsste man einigen Patienten die Opioide vorenthalten, was ethisch kaum zu rechtfertigen wäre.
So hilfreich Opioide sind – sie bergen auch Risiken. Das zeigt sich an der sogenannten Hyperalgesie, dem Phänomen, dass nach einiger Zeit die Schmerzempfindung sogar verstärkt werden kann. Gefördert wird dieser Effekt durch einen abrupten Entzug. Eine Gruppe um Jürgen Sandkühler von der Medizinischen Universität Wien hat herausgefunden, dass hierbei Kalzium-Ionen über bestimmte Rezeptorkanäle in die Nervenzellen der Schmerzbahn im Rückenmark strömen. Möglicherweise verursachen auch starke Schwankungen des Opioidspiegels während der Therapie eine Hyperalgesie. „Darum ist der Einsatz retardierter Darreichungsformen, die den Wirkstoff gleichmäßig über einen längeren Zeitraum abgeben, besonders wichtig“, sagte Sandkühler.
Patienten, die wegen Schmerzen in die Sprechstunde kommen, haben mehr Rechte, als sie und die Ärzte oft glauben. Darauf wies Klaus Kutzer, ehemals Vorsitzender Richter am Bundesgerichtshof, in Frankfurt hin. Er verdeutlichte, „dass es ein allgemeines Menschenrecht ist, von Schmerzen befreit zu werden und, wo dies nicht möglich ist, Schmerzlinderung zu erfahren“. Zudem gebe es hierzulande ein Grundrecht auf eine entsprechende Behandlung. Unter Bezug auf das jüngste Urteil zur Sicherung des Existenzminimums von Hartz-IV- Empfängern sagte Kutzer, die Bekämpfung schwerer Schmerzen sei „genauso ein Aspekt des menschenwürdigen Existenzminimums wie der Erhalt der zum Lebensunterhalt benötigten Geldmittel“. Unterlassene Schmerztherapie könne sogar Körperverletzung sein, denn „das Unterlassen ist dem Tun gleichzustellen, wenn die Pflicht besteht, Schmerzen zu beseitigen“.
Eine Vorreiterrolle beim konsequenten Schmerzmanagement will jetzt die Stadt Münster einnehmen. Dort wurde an diesem Dienstag ein Forschungsvorhaben der Paracelsus Medizinischen Privatuniversität Salzburg vorgestellt, das auf die umfassende Dokumentation und Verbesserung der stationären sowie ambulanten Versorgung zielt. Das Projekt „Aktionsbündnis Schmerzfreie Stadt Münster“ ist auf drei Jahre angelegt.
Text: F.A.Z.
Bildmaterial: Mark Nesbitt and Delwen Samuel, 1988
Die verbreitete Ansicht, dass Opioide sich nicht in ihrem Risikoprofil unterscheiden, muss möglicherweise revidiert werden. Ergebnissen einer Kohortenanalyse zufolge könnte eine länger andauernde Therapie mit Codein das kardiovaskuläre Risiko erhöhen, das Sterberisiko unter Codein und Oxycodon könnte steigen.
Immer wieder werden Ärzte aufgefordert, auch bei schweren, nicht tumorbedingten Schmerzen Opioide einzusetzen. Dabei ist, anders als bei nichtsteroidalen Antirheumatika, wenig darüber bekannt, wie die Risiken der einzelnen Opioide im Vergleich aussehen und ob die Annahme, dass sich Opioide in ihrem Risikoprofil ähneln, richtig ist. Deshalb wurden in einer amerikanischen Kohortenanalyse die Opioide Codein, Hydrocodon, Oxycodon, Propoxyphen und Tramadol im Hinblick auf ihr Risiko für Frakturen, kardiovaskuläre Ereignisse, gastrointestinale Komplikationen und die Sterblichkeit verglichen. Dazu wurden 6.275 Patienten nach dem Propensity-score-matched-Verfahren den fünf Opioid-Gruppen zugeordnet.
Kardiovaskuläre Ereignisse traten 30 Tage nach Behandlungsbeginn in allen Gruppen ähnlich häufig auf, waren jedoch nach 180 Tagen unter Codein erhöht (RR, 1,62; 95% CI, 1,27 – 2,06). Das Frakturrisiko war im Vergleich zu Hydrocodon nach 30 Tagen Einnahme von Tramadol und Propoxyphen signifikant reduziert. Keine Unterschiede wurden im Hinblick auf gastrointestinale Komplikationen gefunden. Dagegen war die Gesamtsterblichkeit im Vergleich zu Hydrocodon nach 30 Tagen Oxycodon-Therapie 2,4-fach, nach Codein-Therapie 2,05-fach erhöht. Die Autoren diskutieren, dass das erhöhte Sterberisiko in Zusammenhang mit kardiovaskulären Ereignissen stehen könnte oder aber auf weitere, nicht erfasste Confounder zurückzuführen ist. Insgesamt muss nach den Ergebnissen dieser Studie davon ausgegangen werden, dass sich Opioide in ihrem Risikoprofil unterscheiden. So ist bei Codein ein erhöhtes kardiovaskuläres Risiko bei längerer Anwendung nicht auszuschließen. Dieses Ergebnis ist überraschend und muss nach Ansicht der Autoren in weiteren Studien validiert werden.
Quelle: Salomon DH et al.: The Comparative Safety of Opioids for Nonmalignant Pain in Older Adults. Arch Intern Med 2010; 170(22): 1979-1986
Ketamine administered intraoperatively in very small doses reduces postoperative opioid consumption. We suggest that this effect is the result of attenuation of acute tolerance to the analgesic effect of opioids. We sought to demonstrate that acute tolerance induced by alfentanil infusion can be attenuated by a dose of ketamine that is too small to produce a direct antinociceptive effect. The experiments were conducted in rats with the use of an infusion algorithm designed to maintain a constant plasma level of the opioid for 4 h. The degree of acute tolerance was determined on the basis of decline in the level of analgesia measured with a tail compression test. Ketamine (10 mg/kg) did not change the baseline pain threshold and did not increase the peak of alfentanil-induced analgesia. At the same time, it attenuated the development of acute tolerance to analgesia during alfentanil infusion and suppressed rebound hyperalgesia observed the day after the infusion. These effects were similar to those observed with dizocilpine (0.1 mg/kg). The development of acute tolerance to analgesia induced by the infusion of an opioid can be attenuated by ketamine administered in doses that are not large enough to provide a direct antinociceptive effect. Therefore, ketamine has the potential to reduce opioid consumption even in subanalgesic doses.
Implications: Ketamine attenuated the development of acute tolerance to analgesia during alfentanil infusion and suppressed rebound hyperalgesia observed the day after the infusion.
The idea of combining an N-methyl-d-aspartate (NMDA) receptor antagonist, inhibiting pain-induced central hypersensitivity, with an opioid (1) has stirred considerable interest in analgesia research. Ketamine as a clinically available NMDA receptor antagonist has been especially attractive in this regard. The authors of a recent review summarizing studies on combined ketamine-opioid administration in postoperative pain concluded that results on the ability of ketamine to improve opioid analgesia are rather contradictory (2). Sethna et al. (3) demonstrated only simple additivity in the effects of ketamine and alfentanil on experimental pain in volunteers. The analgesic effect of ketamine in postoperative pain was observed when the drug was used in a dose range from 0.3 to 0.5 mg/kg, and the effect lasted only for 40 to 60 min (4–6).
Some of the clinical studies (7–9) revealed that ketamine administered during surgery reduced postoperative opioid consumption. These authors used small doses of ketamine (75–150 μg/kg) that could not provide analgesic concentrations in the biophase during the postoperative period. The reduction of opioid consumption was explained by the effect of ketamine on pain-induced central sensitization (7–9). An alternative explanation could be based on the ability of NMDA receptor antagonists to inhibit acute tolerance to the analgesic effect of opioids. We have reported previously (10) that the NMDA receptor antagonist dizocilpine attenuates the development of acute tolerance to analgesia induced in rats by IV infusion of alfentanil. This outcome is similar, although not identical, to the results reported in studies on chronic tolerance in which NMDA receptor antagonists (11–13) or NMDA receptor defect (14) blocked tolerance to the analgesic effect of morphine. Suppression of acute tolerance to alfentanil by dizocilpine, which does not have an analgesic effect by itself, indicates that the direct analgesic effect of ketamine and its effect on opioid-induced analgesia are not necessarily related: the opioid-induced analgesia could be enhanced by the effect of ketamine on opioid acute tolerance that reveals itself in relatively small subanalgesic doses.
Our principal purpose was to test the hypothesis that acute tolerance induced by alfentanil infusion can be attenuated by ketamine in a dose that is not large enough to provide a direct antinociceptive effect. With this aim, it will be possible to substantiate an approach to the treatment of postoperative pain that was actually used in a few clinical studies with ketamine, but the mechanism of ketamine-induced potentiation of opioid analgesia was not identified correctly. The potential of NMDA receptor antagonists to reduce acute tolerance to opioids may be a basis for a novel and important contribution to the relief of postoperative pain. An additional purpose of our study was to examine the effect of ketamine on another opioid-induced adaptive response-delayed hyperalgesia that follows the alfentanil infusion.
Experiments were performed on male Sprague-Dawley rats weighing 320–370 g. The animals were housed with a 12-h light-dark cycle, and food and water were available ad libitum. The protocol for this study was approved by the Institutional Panel on Laboratory Animal Care.
A catheter for the drug infusion was chronically implanted into the jugular vein, and its free end was exteriorized through the skin at the back of the neck. The surgical procedure for implantation was performed under pentobarbital (55 mg/kg intraperitoneally [IP]) anesthesia several days before the experiment. Alfentanil was infused with a Harvard Apparatus pump (model 55–2222; Harvard Apparatus Co., Natick, MA). Alfentanil infusion algorithm was based on the constants of one compartment model for rats derived from our previous study (15).
The responses to mechanical noxious stimulation were determined by measuring the threshold of motor response to increasing pressure applied to the tail—tail compression test (16) with the use of an Analgesy-Meter® (Ugo Basile, Milan, Italy). The rat’s tail was positioned on a Teflon platform, and the pressure plate (0.7-mm edge) attached to this device was applied to the tail while the rat was held in the experimenter’s hand. Pressure was increased at a constant rate (cutoff pressure of 2.375 kg) until coordinated struggle occurred. Three consecutive measurements were recorded, and the mean of the last two measurements was taken as the pressure threshold. For each consecutive determination of the pain threshold, the pressure plate was moved 2-mm cephalad. Measurements were made by an experimenter who was unaware of expected changes in the reaction thresholds among the treatment groups.
Animals were randomly divided into four groups: Alfentanil-Ketamine, Alfentanil-Dizocilpine, Alfentanil-Saline (bolus), and Saline (infusion)-Ketamine, each consisting of eight rats. In all groups, alfentanil was administered as described previously (15,17): a bolus dose of 50 μg/kg followed by an infusion rate of 155 μg · kg−1· h−1 for 4 h. This pattern was chosen to rapidly achieve and maintain a stable alfentanil plasma concentration. The degree of acute tolerance was determined on the basis of decline in the level of pressure threshold during the infusion period. After the alfentanil administration, the pressure threshold was measured twice: 1.5 h and 23 h after the infusion. The last measurement was made to determine the rebound hyperalgesia after the alfentanil infusion. According to preliminary experiments, the measurements made the next day revealed the maximal rebound hyperalgesia that disappeared in a few days after the infusion.
The interacting drugs were administered IV with the first injection given 60 min before the beginning of alfentanil infusion. The following doses were used: ketamine 10 mg/kg (Alfentanil Infusion-Ketamine Bolus Group); dizocilpine 0.1 mg/kg (Alfentanil Infusion-Dizocilpine Bolus Group); isotonic saline (Alfentanil Infusion-Saline Bolus Group); and ketamine 10 mg/kg (Saline Infusion-Ketamine Bolus Group).
The selection of the dose of ketamine was based on the preliminary experiments in which it was verified that 10 mg/kg was not providing an analgesic effect immediately after the drug injection. To further reduce the probability of some direct analgesic influence by ketamine, the interval between the injection of ketamine and the start of alfentanil administration was extended to 1 h. In the rat, ketamine 60 mg/kg IM provides incomplete analgesia, and only at doses of 100 to 120 mg/kg IP can it provide a complete anesthetic effect (18). A more specific NMDA receptor antagonist, dizocilpine, was used in a dose of 0.1 mg/kg.
In the above doses, neither ketamine nor dizocilpine produced behavioral effects interfering with the pressure threshold measurements. The interacting drugs were also administered 5 min after the last measurement of the pressure threshold on the day of alfentanil infusion (second administration) and on the next day, 19 h after the end of alfentanil infusion (third administration), both in the same dose as the first injection (see schedule for drug administration in Table 1).
Effect of Ketamine on Acute Tolerance and Rebound Hyperalgesia Induced by Alfentanil Infusion
The pressure threshold in each of the groups was determined before, and 5 min after, the administration of an interacting drug, at 30, 60, 120, 180, and 240 min after the beginning of alfentanil infusion, and at 1.5 and 23 h after the end of alfentanil infusion. Racemic ketamine hydrochloride was from Parke-Davis (Morris Plains, NJ), dizocilpine maleate (MK-801) was from Sigma Chemical Co. (St. Louis, MO), and alfentanil hydrochloride was from Taylor Pharmaceuticals (Decatur, IL).
The pressure threshold was treated as a continuous variable and was analyzed using a two-way (groups and time) analysis of variance with time treated as a repeated measures factor. Comparisons among groups at each time were performed with the use of an one-way analysis of variance. Multiple comparisons among pairs of means were made by using the Fisher’s protected least significant difference method (19). Differences were declared statistically significant if P < 0.05.
Table 1 shows a summary of the data obtained in all four groups of experiments. The comparison of the pressure threshold before, and 5 min after, ketamine administration (10 mg/kg) indicates that ketamine had no significant analgesic effect. Because alfentanil administration was started 60 min after the ketamine injection, the presence of any direct analgesic effect of ketamine at that time would be even less likely. Dizocilpine also did not produce any changes in the pressure threshold measured 5 min after its injection.
The effect of ketamine on acute tolerance to alfentanil is illustrated by Figure 1, which shows a comparison of the alfentanil-induced changes in the pressure threshold. It demonstrates (A segment) that, in the Alfentanil-Saline Group, the pressure threshold before the end of alfentanil infusion was only insignificantly more than that before the start of infusion (808 ± 78 g vs 733 ± 66 g, not significant). At the same time, in the Alfentanil-Ketamine Group, the pressure threshold at the end of alfentanil infusion was much higher than that before the start of infusion (1078 ± 191 g vs 763 ± 64 g, P < 0.001); and it was higher than in the Alfentanil-Saline Group at the same time interval (1078 ± 191 g vs 808 ± 78 g, P < 0.05). The changes in the Alfentanil-Dizocilpine Group were similar to those in the Alfentanil-Ketamine Group. The Saline-Ketamine Group demonstrated a constant pressure threshold level for the whole study period.
Figure 1. The effect of ketamine on acute tolerance to continuously infused alfentanil. Alfentanil was administered as a bolus of 50 μg/kg followed by a constant-rate infusion at 155 μg · kg−1 · h−1 for 4 h. Ketamine was injected in a dose of 10 mg/kg IV 60 min before the start of alfentanil administration. A, Alf + Sal = alfentanil infusion and isotonic saline as an interacting drug; Alf + Diz = alfentanil infusion and dizocilpine 0.1 mg/kg IV 60 min before alfentanil; Alf + Ket = alfentanil infusion and ketamine 10 mg/kg IV 60 min before alfentanil; Sal + Ket = isotonic saline infusion and ketamine 10 mg/kg IV 60 min before the start of saline infusion. Each dot reflects a mean ± sd for a group of eight rats at various time intervals. *P < 0.05, +P < 0.01, both versus value at 30 min in each of the groups. B, Changes in cumulative reductions of the initial analgesic effect. Columns represent reductions in percent (mean ± sd). Cumulative reduction of the initial analgesic effect was calculated by comparing the alfentanil-induced increase in pressure threshold (from predrug baseline value) at 30 min of the infusion (initial analgesic effect) with the increases from the predrug baseline separately at 60, 120, and 240 min (gradual cumulation of the effect). *P < 0.05 versus corresponding value of Alf + Sal group.
The effects of ketamine and dizocilpine for reduction of the initial analgesic response at various time intervals during alfentanil infusion are presented in Figure 1B. Both drugs significantly (P<0.05) attenuated tolerance development at all time intervals as presented by cumulative reduction of the initial analgesic effect (explanation in the legend to Figure 1B). The effect of dizocilpine had a tendency to be more pronounced than that of ketamine, although this tendency did not reach statistical significance.
In addition to the attenuation of acute tolerance to alfentanil, ketamine inhibited the alfentanil-induced rebound hyperalgesia. After the 4-h alfentanil infusion, there was a decrease in the pressure threshold that reached its maximum the day after infusion and then gradually returned to the baseline level, usually 1–2 days later. Table 1 indicates that in the Alfentanil-Saline Group, 23 h after the end of alfentanil infusion, the pressure threshold was decreased 27% from baseline level (532 ± 65 g vs 733 ± 66 g, P < 0.001). In the Alfentanil-Ketamine Group, animals received three injections of ketamine 10 mg/kg (60 min before the start of alfentanil infusion, and 5 min and 19 h after its end). This treatment resulted in a decrease of the pressure threshold decline 23 h after the end of alfentanil infusion (539 ± 65 g in Alfentanil-Saline Group vs 692 ± 54 g in the Alfentanil-Ketamine Group, P < 0.001). Figure 2 shows a comparison of the degree of the rebound hyperalgesia with and without the NMDA receptor antagonist’s administration. Both ketamine and dizocilpine suppressed it, with dizocilpine completely suppressing it; however, statistical significance (P = 0.058) of the difference between the Dizocilpine and Ketamine Groups did not reach the accepted level of P value.
Figure 2. Effect of ketamine on rebound hyperalgesia induced by alfentanil infusion. Columns represent reductions of pressure thresholds (percent of baseline value, mean ± sd) 23 h after the end of the 4-h alfentanil infusion. Animals received three injections of interacting drugs in equal doses: 60 min before the start of alfentanil infusion, and 5 min and 19 h after its end. Ketamine was used at a dose of 10 mg/kg, and dizocilpine at a dose of 0.1 mg/kg. *P < 0.001 versus corresponding value of the alfentanil (Alf) + isotonic saline (Sal) group.
Both alfentanil-induced adaptive changes assessed in the present study—acute tolerance and rebound hyperalgesia—were attenuated by ketamine. The development of acute tolerance to the antinociceptive effect of alfentanil was decreased by ketamine at all time-intervals of the four-hour alfentanil infusion. The ability of ketamine to attenuate chronic tolerance to morphine was reported with systematic and intrathecal drug administration in rodents (20–22).
In our experiments, ketamine 10 mg/kg was administered IV one hour before the beginning of alfentanil infusion. The baseline pressure threshold measured five minutes after ketamine was not changed (Table 1), and the peak of the alfentanil-induced antinociceptive effect with ketamine pretreatment was the same as that with the saline pretreatment (Table 1 and Figure 1A). These results indicate that the dose of ketamine we used was not large enough to provide a direct antinociceptive effect, even in combination with alfentanil. Similar results with systemic ketamine 10 mg/kg were reported in mice: ketamine did not change the response to mechanical or thermal nociceptive stimuli (23). Also, when ketamine 10 mg/kg was administered with morphine in rats, the morphine dose-response curve was not changed to any significant degree (21). With phasic pain, ketamine provides analgesia only in very large doses (24). That agrees well with the fact that, in rats, only at doses 100 to 120 mg/kg IP does it block motor nociceptive responses in minor surgical procedures (18).
The pattern of ketamine biodisposition is characterized by a very rapid redistribution from the brain to other tissue (25). In the rat, 60 minutes after an IV ketamine injection, its brain level declined 20-fold compared with the level measured immediately after the injection (26). This indicates that when attenuation of acute tolerance to alfentanil occurred (two to five hours after ketamine bolus injection), in our experiments, the ketamine biophase concentration was at least 20-fold smaller than that immediately after the injection. Thus, despite the fact that the ketamine concentration was too small to produce a direct antinociceptive effect, it effectively attenuated the development of acute tolerance to alfentanil.
Bilsky et al. (12) reported that NMDA receptor antagonists blocked chronic antinociceptive tolerance to morphine, but not however, to selective μ or δ agonists, including fentanyl. They concluded that the effect of NMDA receptor antagonists on opioid tolerance is not a general phenomenon related at all opioids. Alfentanil, used in our study, belongs to the same group of opioids as fentanyl. The difference in the results is probably related to the difference in the model of tolerance (chronic versus acute).
Rebound hyperalgesia that was present the day after the alfentanil infusion was also attenuated by ketamine. This confirms similar observations with delayed hyperalgesia induced by multiple bolus injections of fentanyl (27). The rebound hyperalgesia observed during opioid abstinence could result from reduction of a tonic inhibitory modulation that was present before opioid administration; however, the activation of modulatory neurons that facilitate nociceptive transmission could also be involved (28).
Ketamine is a nonspecific noncompetitive NMDA receptor antagonist; however, its effects on acute tolerance to alfentanil and on delayed hyperalgesia were almost the same as those of dizocilpine, a specific noncompetitive NMDA receptor antagonist. The effects of dizocilpine were only insignificantly more pronounced than those of ketamine.
The activation of NMDA receptors in the central nervous system is seen as a mechanism involved in the adaptive changes underlying both tolerance to opioids and delayed hyperalgesia. It was suggested that activation of opioid receptors leads to protein kinase C-mediated activation of NMDA receptors (29,30). The attenuation of acute tolerance and rebound hyperalgesia by the NMDA receptor antagonists is in agreement with this suggestion.
Could our results be relevant to the clinical experience with acute opioid exposure in surgery? The tolerance to analgesia during remifentanil infusion in humans is profound and develops very rapidly (31). Chia et al. (32) reported that the preoperative and intraoperative use of fentanyl in large doses (15 μg/kg plus 100 μg/h for 2–3 h) resulted in an increased postoperative fentanyl consumption via patient-controlled analgesia (up to 50%) and increased pain severity compared with preoperative administration of a small dose of fentanyl (1 μg/kg). It was also found that patients who received more morphine during the initial postoperative period had increased opioid requirements for pain relief after the initial period (33). In a recent editorial, Eisenach (34) concluded that we may be contributing to postoperative pain by the use of large doses of opioids intraoperatively. Thus, attenuation of the development of acute tolerance to opioids could be a clinically important approach for the treatment of postoperative pain, and the possible role of ketamine in this regard deserves specific attention.
The value of ketamine in the treatment of postoperative pain is a very controversial issue (2,25). To provide a direct analgesic effect, ketamine should be used in relatively large doses, which is associated with significant adverse effects. However, several authors (7–9) reported that ketamine administered during surgery in small doses (75–150 μg/kg) reduced postoperative opioid consumption. We hypothesize that this effect is the result of attenuation of acute tolerance to opioids. Figure 3 illustrates this suggestion by presenting three antinociceptive effects of ketamine that require different concentrations of the drug. Attenuation of tolerance to the analgesic effect of opioids occurs at the smallest concentration. Therefore, ketamine in subanesthetic (effect on phasic pain) or subanalgesic (effect on tonic pain) doses can still reduce opioid consumption.
Figure 3. Hypothetical dose-response relationship for the effects of ketamine related to nociception.
There is a separate pharmacologic property of ketamine that is related to the treatment of postoperative pain. NMDA receptor antagonists, including ketamine, can prevent the induction of injury-induced central sensitization and abolish hypersensitivity to pain once it is established (35). This property is a basis for the use of ketamine for preemptive analgesia (2). In a study on surgical patients, we could not demonstrate the preemptive effect of ketamine (used in a large dose of 2 mg/kg bolus + 20 μg · kg−1 · min−1 infusion during surgery) on spontaneous or movement-induced pain; however, its effect on hyperalgesia to pressure on the wound was observed even 48 hours after the surgery (36). The effect of ketamine on pain-induced central sensitization could be a factor in the decrease of postoperative pain, and consequently, in the reduction of opioid requirements (7–9). This study suggests that the ketamine-induced attenuation of acute tolerance to opioids might also be a potentially beneficial mechanism in the treatment of postoperative pain resulting in reduction of opioid requirements. It is interesting that mechanisms underlying injury-induced central sensitization and opioid-induced tolerance have close relationships. Mao et al. (30) suggested that these two seemingly unrelated phenomena may have common neural substrates that interact at the level of excitatory amino acid receptor activation and related intracellular events.
In conclusion, ketamine attenuated the development of acute tolerance to analgesia during alfentanil infusion and suppressed rebound hyperalgesia observed the day after the infusion.
Supported by National Institutes of Health Grant GM35135.
source: http://www.anesthesia-analgesia.org/content/91/6/1483.full
Russia is the world’s largest heroin consumer and, to add to that, risky injecting practices have fuelled one of the world’s fastest-growing HIV epidemics. With tens of thousands of people dying every year, in a country where the population is shrinking, the twin epidemics are a catastrophe.
Campaigners say methadone would help tame both the heroin and HIV epidemics. As well as preventing HIV transmission, giving addicts methadone also brings them into the medical system, help steer them away from committing crimes to fund their habit and takes trade away from illegal dealers. Even China uses the technique to treat drug addicts. But Russian officials will have none of it. Government figures say it is perverse to treat drug addiction with other drugs and favour methods based on full withdrawal, sometimes against an addict’s will. It’s risky even to discuss methadone – advocates can be accused of „pro-drugs propaganda“ and taken to court.
„There is no logical reason behind Russia’s opposition to substitution therapy,“ says Anya Sarang, a campaigner who advocates the introduction of methadone. „I’ve been fighting this battle for 12 years and I don’t understand the mentality at all. The scientific evidence is all there to prove that it works.“
Ms Sarang and a group of Western academics published a study in the British Medical Journal last year which found that the widespread introduction of substitution therapy could cut rates of HIV transmission in Russia by up to 55 per cent. Estimates vary, but it’s thought that more than two million Russians inject heroin and the drug causes 30,000 deaths per years, as well as tens of thousands of new HIV cases. Russia is located on the transit route for drugs from Afghanistan to Europe and cheap heroin is readily available – a dose of heroin on the streets costs about 600 roubles (£12). If methadone therapy is not available, activists say programmes that offer addicts clean needles and syringes to avoid HIV transmission are essential.
The government, however, is adamant that only aggressive punitive measures can work to tackle drug use. Needle-exchange programmes funded by foreign donors have been discontinued in recent years, leading many addicts to share injecting equipment.
While there is some discussion about whether needle exchanges should be reintroduced, methadone is completely taboo. Leading Russian drugs specialists denounce substitution therapy as a failed Western imposition and see it as a „legalisation“ of drug use.
„We have no evidence from the international community that methadone is effective,“ said the Health minister, Tatyana Golikova, this week, reiterating a long-held government policy.
Others go further. Evgeny Roizman is a former Russian MP from the city of Yekaterinburg in the Ural mountains. He runs a series of clinics there where drug addicts go cold turkey, without methadone or any other drugs to ease the withdrawal symptoms.
He insists that methadone advocates are simply being disingenuous. „These people will say anything to get Western funding,“ says Mr Roizman. „I have worked with drug addicts for years, and I can tell you: methadone doesn’t work.“
He wants to bring in a range of policies, including harsher penalties for drug dealers and compulsory drugs testing in all Russian schools and colleges. „We need forced treatment for drug addicts,“ he says. „We need to force them into special institutions where there are no drugs and where they can be treated. This is the answer, not methadone.“
Last year, a disciple of Mr Roizman was sentenced to three-and-a-half years in prison for kidnapping drug addicts. Yegor Bychkov said addicts‘ parents had given him permission to „cure“ their children. „Patients were tortured, chained up to steel beds, starved,“ says Ms Sarang. „It was absolutely outrageous and when the court case against him started, we thought there would be a scandal.“
But a huge wave of support for Mr Bychkov swept through the country. Even many from Russia’s beleaguered human rights community joined with church figures and government officials to condemn his trial and in the end the court suspended his sentence and he was released. Mr Bychkov was „overenthusiastic“, said Mr Roizman, but his heart was in the right place.
Ms Teplinskaya, who is still a heroin user, travelled to Moscow last week to meet Navi Pillay, the UN High Commissioner for Human Rights, and ask her to press the Russian government on substation therapy. „I think I could have done a lot of good things for my country,“ she said. „But instead, I’ve lost my home, my health and my family. Methadone could have helped me lead a normal life.“
But her opponents are confident their views will prevail. Mr Roizman says: „They can shout as much as they want with their Western money. Methadone will never be legal in Russia.“
MOSCOW, Feb 10 (Reuters) – Activists have asked the UN human rights
chief to pressure Russia to legalise the heroin substitute methadone when she visits next week amid a worsening HIV/AIDS crisis, an international health group said on Thursday.
UN High Commissioner for Human Rights Navi Pillay will meet President Dmitry Medvedev, government officials and around 60 rights campaigners during a five-day visit to Moscow.
‚This is a national health crisis and a human rights priority in Russia that must be raised at the highest levels,‘ said senior human rights analyst Damon Barrett from the London-based International Harm Reduction Association (IHRA).
The IHRA and 16 other HIV-focused rights organisations have sent a letter to Pillay asking her to push for HIV/AIDS and drug-fighting measures including the introduction of methadone, during her meetings with Russian government.
The UN’s World Health Organisation (WHO) says Russia has one of the fastest growing HIV/AIDS epidemics in the world, fueled up to three million heroin addicts, many of whom use dirty needles, local health organisations say.
Unlike most countries, Russia refuses to finance harm reduction programmes such as needle exchanges, or to legalise the replacement drug methadone.
The Health Ministry says there is no proof methadone is effective, while the country’s top doctor Gennady Onishchenko has called methadone ‚just another narcotic‘.
‚The fact that the government’s policy is so incomprehensible is what makes it so frustrating,‘ Barrett said.
The WHO says there are a million HIV-positive people in Russia, and deems methadone essential in fighting the epidemic.
Pillay will meet Russian activist Irina Teplinskaya during her visit, said the Moscow-based Andrey Rylkov Foundation, for whom Teplinskaya volunteers. HIV-positive and a heroin user, Teplinskaya has become a symbol of Russia’s drug woes.
‚Because there is no opioid substitution therapy in Russia, drug-dependent people are not able to receive treatment for HIV… they are forced to spend whole days acquiring money in a criminal way so they can buy drugs,‘ Teplinskaya said in a speech she will deliver to Pillay on Sunday.
((For a special report on Russia’s heroin and HIV/AIDS problem: ))
LONGVIEW — Amy Lynn Cowling was 33, she had three children, and her first grandchild was born a day after she died in an East Texas jail — slumped over her bed, clutching a bottle of Diet Dr Pepper, after a day of wailing and seizures.
Ms. Cowling was pulled over on Christmas Eve for speeding and arrested for outstanding warrants on minor charges. She was bipolar and methadone-dependent and took a raft of medications each day. For the five days she was in Gregg County Jail, Ms. Cowling and her family pleaded with officials to give her the medicines that sat in her purse in the jail’s storage room. They never did.
Ms. Cowling’s death is the most recent at Sheriff Maxey Cerliano’s Gregg County Jail in Longview. Since 2005, nine inmates have died there — most were attributed to health conditions like cancer, diabetes and stomach ulcers — far more than at other facilities its size. Bowie County Jail, in East Texas on the Arkansas border, reported five deaths in the same period, as did Brazoria County Jail, south of Houston on the Gulf Coast. In Williamson County in Central Texas near Austin, the jail reported just two deaths.
Interviews with prison experts and people with firsthand experience with the Gregg County lockup and its medical staff, as well as a review of scores of public documents, reveal a troubled local jail where staff turnover is high and inmates routinely complain about conditions. Criminal justice advocates say the situation in Gregg County is not unique; it is representative of systemic problems that plague local jails statewide.
Sheriff Cerliano defends the medical treatment in his jail and said he does his best to weed out bad jailers. “It’s only about doing the right thing,” he said.
Vicki Bankhead never went a day without talking to Ms. Cowling, her daughter and best friend. “I miss hearing her voice,” Ms. Bankhead said, sobbing. Ms. Cowling became a mother at age 15. She had become addicted to prescription pills and was found guilty in 2001 of possessing a fraudulent prescription. She struggled to keep a job.
Although Ms. Cowling had been clean for several years and was getting treatment at a methadone clinic, Ms. Bankhead said, her daughter had other health problems, including bipolar disorder, heart troubles and a failing kidney. “Amy needed her medication to stay alive,” she said. “That’s why I was begging them to help her repeatedly.”
Public records show that Ms. Cowling told Gregg County Jail officials that she had high blood pressure, arthritis and only one kidney. She reported that she took Seroquel to treat bipolar disorder and that she had been receiving methadone treatment for a decade — but neither of those drugs is allowed in the jail.
State standards require only that jails provide treatment according to the facility’s health care plan. Dr. Lewis A. Browne, the county health administrator and jail doctor since 1992, decides which drugs are allowed. Drugs like Seroquel and methadone, he said, are often traded among inmates for illicit favors.
Gregg County officials said that Ms. Cowling had received appropriate substitute medications.
Reports on her case submitted to the Texas attorney general’s office show that Ms. Cowling began having “seizure activity” while she was in the facility. The morning before she died, a jail nurse called Dr. Browne to report that Ms. Cowling was “hollering and uncooperative.” Dr. Browne told the nurse to give Ms. Cowling a dose of the antipsychotic drug Haldol. When a nurse called Dr. Browne later to report that Ms. Cowling was yelling again, he ordered more Haldol and put her on suicide watch. Ms. Cowling was booked on a Friday morning, and a jailer discovered her dead just after midnight on Wednesday.
Precisely what caused Ms. Cowling’s death remains unknown. A preliminary autopsy was inconclusive. Her family has retained a lawyer.
County officials contend that Ms. Cowling’s death was not their fault. She was not honest with them about all of her health problems, said Robert Davis, a lawyer for the county. “I absolutely do not believe that the jail or jail staff contributed to this inmate’s death whatsoever,” Mr. Davis said.
Sheriff Cerliano, however, concedes that not everything went according to the jail’s policies. After Ms. Cowling’s death, he conducted an investigation that he said showed that one jailer falsified observation logs that night. He fired five jailers and a sixth resigned. (Not all of the firings were related to Ms. Cowling’s death, he said, but were for conduct discovered during the investigation.) Two of the jailers were arrested for falsifying government documents.
Still, he said, the jail staff followed medical protocol in caring for Ms. Cowling. “We do everything we can to take care of inmates,” he said.
Since 2008, Gregg County inmates have filed more than 20 complaints with the Texas Commission on Jail Standards about conditions in the lockup. Most of the complaints were health-care-related; inmates said they could not get medicine and did not receive timely medical attention. An inmate who hanged himself in the jail in 2009 had complained that among many other grievances, he was not allowed medication he had been prescribed on the outside and had not been seen by a doctor.
In letters responding to nearly all the complaints, Adan Muñoz, the commission’s executive director, wrote, “The Texas Commission on Jail Standards does not question the professional opinion of medical personnel.”
Inmates have sued Sheriff Cerliano and Dr. Browne at least twice since 2005, alleging that their constitutional rights were violated by the jail’s deliberate indifference to their medical needs. In both cases, the courts found that Dr. Browne and the jail had attempted to provide adequate care.
Dr. Browne, who has his own family medical practice in Longview, is paid more than $100,000 per year to act as the jail doctor and director of the county health authority. He said that inmate health care was “the toughest medical situation to deal with.” Inmates are often uncooperative and dishonest about their health conditions, he said, and many are drug addicts. Adding to the challenge is that it is hard to retain medical staff, Dr. Browne said.
Medical staff members at the jail are not the only ones with a high turnover rate; records from the sheriff’s department show that in 2009 and 2010, more than 40 percent of the 167 jail employees either quit or were fired.
Sheriff Cerliano said the pay is low for jailers and that they have to go through months of training, pass drug screenings and work in challenging situations.
Lt. David Drosche, who works in the Brazos County Sheriff’s Office and is president of the Texas Jail Association, agreed that retaining jailers is difficult but said that a 40 percent turnover rate is “extremely high.” The higher turnover, he said, results in more inexperienced jailers.
County lockups in Texas are accountable to the Texas Commission on Jail Standards. Before Ms. Cowling’s death, the Gregg County Jail had passed every commission inspection for the last five years. Within weeks after she died, the commission, which reviews county jail deaths, decided the jail was in compliance with state standards.
But the commission does not require that jails meet specific health care criteria, only that they have medical plans on file. It also doesn’t keep track of jail staff turnover.
Diana Claitor, executive director of the Texas Jail Project, which advocates for improved jail conditions, said better health care standards and monitoring of data like staff turnover could help prevent more deaths like Ms. Cowling’s. From January 2005 to September 2009, more than 280 inmates died from illnesses in Texas county jails.
“One of the chief factors playing into mistreatment or neglect would be ill-trained, inexperienced staff,” she said. But with the state budget crunch, pressing the jail standards commission to provide additional oversight is a tough sell, Ms. Claitor said.
Sheriff Cerliano said his jailers already receive more training than is required by state standards and that the medical staff provides the best care possible. Ms. Cowling’s death was unfortunate, he said, but it does not mean that wholesale changes are needed in the way jails are regulated.
“We do have inmates that come in sick,” he said. “It’s incumbent upon us to try to do the best we can.”
Geld aus Drogengeschäften korrumpieren Regierungen und lösen weltweit Gewalt aus. Warum wir einen pragmatischeren Ansatz zur Bekämpfung brauchen.
Aufgrund der direkten Demokratie in der Schweiz können die Bürger dieses Landes durch das Sammeln von genügend Unterstützungsunterschriften landesweite Referenden über Regierungspolitik und Gesetze veranlassen.
Nach einer Welle von Aids-Todesfällen in den 1980er Jahren, sahen sich die Schweizer mit einem Problem konfrontiert, das in den USA, Russland, Lateinamerika, der Europäischen Union, Südasien und anderen Regionen dieser Welt schon Millionen Menschenleben gekostet hat. Intravenös injizierende Drogenkonsumenten – vor allem Heroinabhängige – hatten öffentliche Plätze in Zürich und anderen Schweizer Städten in so genannte „Needle Parks“ verwandelt. AIDS erwies sich als Krankheit, die offenbar auch vor dem Wohlstand nicht Halt macht.
Die Schweizer reagierten auf das Problem nicht mir jener Art von Nachlässigkeit, mit der die russische Regierung bislang auf ihre Heroin- und HIV-Epidemien reagiert hat – dort gibt es über zwei Millionen Drogenkonsumenten und eine geschätzte Million Menschen mit HIV-Infektion, von denen sich über 60 Prozent durch kontaminierte Nadeln ansteckten. Ebenso wenig reagierten die Schweizer mit einem „Krieg gegen Drogen“ oder mit noch mehr Geld für mehr Polizei, mehr Gefängnisse und zwingende Haftstrafen.
Dieser Krieg ist nämlich endgültig verloren. In den USA sitzen heute mehr Menschen im Gefängnis als in jedem anderen Land und dies ist größtenteils auf die sprunghaft steigende Zahl von Verurteilungen aufgrund von Drogen zurückzuführen, wobei die Zahl afroamerikanischer und hispanoamerikanischer Insassen überproportional hoch ist.
Der Krieg gegen Drogen ermöglichte den Drogenkartellen höhere Profite als jemals zuvor und verwandelte in Lateinamerika ganze Städte in Feudalgebiete. Drogengelder korrumpieren demokratische Regierungen und Institutionen der Gesetzesvollstreckung auf der ganzen Welt. Gewalt im Zusammenhang mit Drogen hat in Afghanistan, Burma, Kolumbien, den USA und Mexiko unzählige Opfer gefordert.
Die Schweizer überprüften die Drogenpolitik ihrer Regierung mit Pragmatismus. Fachleute aus dem medizinischen Bereich übernahmen die Führung einer Kampagne, mit der die Regierung – durch die Mechanismen der direkten Demokratie – dazu gebracht werden sollte, ihren Schwerpunkt von Haft und Strafen für Drogenkonsumenten hin zu einer Gesundheitspolitik zu verlagern, die auf Grundlage wissenschaftlicher Erkenntnisse erhebt, welche Ansätze funktionieren.
Die Schweizer führten Methadonprogramme ein und um die Ansteckung mit HIV zu vermeiden, wurde der Nadelaustausch – auch in Gefängnissen – etabliert. Überdies wurden im großen Maßstab Drogenkonsumräume geschaffen. Das Schweizer Bundesamt für Gesundheit überwachte auch ein Experiment, im Zuge dessen man Heroin an Personen verschrieb, die über lange Zeit von Opiaten abhängig waren.
Die sorgfältige Auswertung dieses Ansatzes durch die Schweizer Regierung zeigte, dass eine heroingestützte Therapie sowohl machbar als auch kosteneffizient ist und dass sie für die Patienten mit signifikanten Verbesserungen der Gesundheit einhergehen kann. Außerdem wurde damit ein Beitrag zu einem erstaunlichen Rückgang der Drogenkriminalität geleistet. Die Schweizer Öffentlichkeit war von den Vorteilen der heroingestützten Therapie so überzeugt, dass die Bürger diese Politik trotz politischer Opposition im eigenen Land und Kritik des Internationalen Suchtstoffkontrollrats in zwei landesweiten Referenden unterstützten.
Die Schweiz ist ein konservatives Land. Der Handel mit Suchtstoffen bleibt weiterhin illegal. Im November 2008 wurde ein Antrag für eine Entkriminalisierung von Cannabis nach holländischem Muster abgelehnt. Und manche politischen Entscheidungsträger fragen sich, ob sich der Schweizer Ansatz in der Drogenpolitik zu sehr auf die öffentliche Gesundheit und zu wenig auf die Bekämpfung von Armut und soziale Ausgrenzung konzentriert, mit der sich die Drogenkonsumenten konfrontiert sehen.
Der pragmatische Ansatz der Schweiz hinsichtlich des Drogenmissbrauchs bietet dennoch wichtige Lehren, die auch auf die USA, Russland und viele andere, von Drogen und HIV/AIDS belastete Länder in deren Einflussbereich angewendet werden können. Ähnlich verhält es sich mit den Erfahrungen in Portugal, das vor einem Jahrzehnt die EU-Rangliste der mit Drogen in Zusammenhang stehenden HIV/AIDS-Fälle anführte.
Die Entscheidung Portugals aus dem Jahr 2001, den Besitz illegaler Drogen zu entkriminalisieren, führte nicht nur zu mehr Drogenkonsumenten in Behandlung (statt im Gefängnis), sondern auch zu einem bedeutenden Rückgang der Ansteckungen von Drogenkonsumenten mit HIV.
Eine Lehre für politische Entscheidungsträger besteht darin, dass es von zentraler Bedeutung ist, die neuen Programme auf Grundlage strenger wissenschaftlicher Überprüfung – und nicht auf Basis populistischer Rhetorik, religiösem Moralismus und Großstadtlegenden – durchzuführen.
Dies erfordert die Koordination von Polizeiarbeit und Gesundheitsprogrammen innerhalb eines einheitlichen Rahmenwerks, Investitionen in Forschung und öffentliche Aufklärung über Drogenpolitik, die Öffnung neuer Programme gegenüber unabhängiger Überprüfung und die Fähigkeit, ideologischer Kritik auf nationaler und internationaler Ebene mit wissenschaftlichen Beweisen und Pragmatismus entgegenzutreten.
Um diese und andere bedeutende Lehren zu vermitteln sowie weltweit für eine effektive, schadensmindernde Politik – sowie eine breitere öffentliche Debatte über effizientere und humanere Drogenpolitik – einzutreten, haben wir gemeinsam mit bedeutenden Persönlichkeiten die Globale Kommission zur Drogenpolitik ins Leben gerufen, die im Januar in Genf ihre Gründungsversammlung abhielt.
Unser Ziel ist zu beweisen, dass der Krieg gegen Drogen verloren ist. Die Schweiz, Portugal und andere Länder haben gezeigt, dass es einen besseren Weg gibt, indem man Pragmatismus und Wirtschaftlichkeit mit Mitgefühl und Respekt vor den Menschenrechten kombiniert.
Fernando Henrique Cardoso war von 1995 bis 2003 Präsident Brasiliens und ist nunmehr Vorsitzender der Globalen Kommission zur Drogenpolitik. Michel D. Kazatchkine ist Geschäftsführer des Globalen Fonds zur Bekämpfung von AIDS, Tuberkulose und Malaria.
Siehe auch https://exilope.wordpress.com/2011/02/04/neue-wege-in-d…-drogenpolitik/
quelle is die Welt: http://www.welt.de/debatte/die-welt-in-worten/article12462030/Der-Krieg-gegen-Drogen-ist-schon-lange-verloren.html
When Charlie Sheen finally entered rehab, it wasn’t terribly shocking news. But what most people did find surprising was that instead of checking into a swanky Malibu treatment center as he has done in the past, Sheen opted to receive in-home rehab. Immediately the media began criticizing his choice and questioning his commitment to getting sober.
There are undoubtedly certain challenges related to in-home rehab, but are you really guaranteed better care if you check into a treatment center?
Absolutely not, thanks to the lack of standardization in our current rehab system.
Each year, about three million Americans seek help from a seemingly endless list of treatment facilities. But who is ensuring these treatment centers are qualified to effectively treat them?
With a lax application process for state licensure and certification, there is little accountability placed on facilities, or their ownership, to ensure proper treatment is being offered. With more than 12,000 rehab centers in the country, the odds of finding the one that best fits your needs are next to impossible.
When treatment fails, which it often does, it is then assumed to be the addict who failed, when in reality it was often the addict who was failed by a flawed system.
This leads to a vicious cycle of relapse — a story all too familiar to families struggling with addiction, not to mention one we’ve seen repeatedly played out by Hollywood stars.
It is true that some don’t take advantage of their treatment and fail at sobriety on their own, but others simply weren’t given a chance to succeed.
This is made worse by the fact that most rehab clinics market themselves as „all inclusive“ — able to treat any type of addiction disorder — which most are certainly not. Addicts and their families are often so desperate to get help that they select a rehab clinic based on cost and availability, without understanding whether or not the care providers are properly certified in the type of addiction that affects them or are qualified to fulfill any additional needs they might have (including mental health needs).
This is especially true of first-timers (over 60 percent of those seeking addiction treatment are first-timers). They don’t know what questions to ask or even what they are looking for out of a treatment center, making it nearly impossible to find the right option for their individual needs.
We need to try and get some measure of standardization into the system so that we are able to match those looking for treatment with providers that fit their needs. Currently, there is essentially no oversight regarding the services addiction treatment providers report and their actual capabilities for providing those services.
In the place of a centralized federal or state-level vetting system, there are some private groups that provide directories. But it is not easy to tell how well these directories actually vet the treatment centers listed. It is critical for treatment candidates to know exactly what type of credentialed treatment services are provided. This should be provided by the public health departments, but until that happens, it’s basically „every man for himself.“ (At my site All About Addiction, we recently launched our own „rehab finder,“ to provide a vetting system in the meantime.)
We believe this is a crucial element for successful treatment; especially when you consider that more than 50 percent of addicts suffer from mental health issues, meaning they need special care by a trained professional. And while some may promise this, there is no verification process to ensure they are able to deliver on their promise.
In fact, a huge survey of the addiction treatment industry found that more than 20 percent of addicts entering treatment were missing crucial mental health services that they needed. (About 50 percent were missing other necessary medical services.)
Rehab is a business — a booming one, at that — and right now it is too easy to sell the idea of recovery. Because there is no model of care to follow, the system is compromised with clinics that don’t know how to do things better, some that limit their treatment due to dogma and other centers that are actually trying to „game“ the system.
The bottom line is, without some level of standardization, treatment becomes nothing more than a crapshoot. You are left at the mercy of a broken system and never know what kind of treatment you are going to receive until it is too late.
Right now, you could easily check into rehab facility and find they offer nothing more than an expensive 12-step program. This is unacceptable. We have tools, like cognitive behavioral therapy and motivational enhancement therapy, which we know are effective, we just need to ensure they are part of the treatment model being offered to patients.
Add to that some very effective, if poorly utilized, medications and it’s clear we’re handicapping our patients, pun and all.
However, there is hope, and a better way of doing things, but it will require us to adopt a more progressive model of treatment.
Our society has too readily accepted the supposed „fact“ that recidivism rates are high, and will always be high, for addicts. The fact of the matter is that the treatment process itself is deeply flawed and until we fix the model of care for recovering addicts, we will never be able to truthfully tell how many of them can recover. Addiction isn’t a death sentence. It is a treatable disease; we need to acknowledge that the way we are doing things doesn’t work and do something to change it.
After many years of trial and error, researchers and doctors have finally begun to grasp what works and what doesn’t in terms of treating addiction.
It is now our job and our responsibility to start developing a system that gets the proper treatment to the people who need it.
Any doctor will tell you, there are no guarantees with addiction. All we can do is give people the best shot at treatment, and sadly, right now, our system is failing at that.
Adi Jaffe,
AlterNet
February 11, 2011
http://www.alternet.org/story/149898/
Adi Jaffe, Ph.D. is a Los Angeles addiction psychologist and researcher. Himself a former drug addict and convicted drug dealer, Dr. Jaffe is an expert on substance abuse, especially on the neuroscience and policy issues involved. Today, he is a UCLA-affiliated researcher on addictions, founder of AllAboutAddiction.com and a columnist for Psychology Today.
© 2011 Independent Media Institute. All rights reserved.
Die Opiat-Substitution gilt als Standardtherapie bei Opiatabhängigkeit.
Neben Methadon, einem Razemat aus den beiden Enantiomeren
Levomethadon und Dextromethadon, kommt dabei in Deutschland seit
20 Jahren auch das Enantiomer Levomethadon zum Einsatz, das in verschiedenenStudien eine bessere Wirksamkeit und Verträglichkeit gezeigt hat.
Im Rahmen der nicht-interventionellen STABIL-Studie (= Studie zur Therapie Opiat-/Opioid-Abhängiger nach Behandlungsumstellung instabiler
Methadon-Patienten auf Levomethadon-Lösung zur Substitution)
wurden opioidabhängige Patienten mit instabilem Behandlungsverlauf
unter dem Methadon-Razemat auf Levomethadon umgestellt.
Die Auswertungen hinsichtlich Verträglichkeit, Suchtdruck und Beikonsum zeigen,dass sich durch die Umstellung der Substitutionsbehandlung auf
Levomethadon bei Patienten mit einem unbefriedigenden Behandlungsverlauf
unter Methadon-Razemat eine signifikante Verbesserung
der Therapie bezüglich Wirksamkeit und Verträglichkeit sowie eine signifikante Verringerung des Suchtdrucks (craving) und des Beigebrauchs
erreichen lässt. Diese Ergebnisse sind vor allem auch deshalb positiv zu
bewerten, weil die meisten Patienten in dieser Studie einen langen
polytoxikomanen Drogenkonsum (im Median 13 Jahre), eine hohe Komorbiditätsrate
und hohen Beikonsum von Drogen, Medikamenten und
Alkohol aufwiesen.
1 EINLEITUNG
Die Opiat-Substitution hat sich, in Deutschland wie auch
weltweit, zur Standardtherapie der Opiatabhängigkeit entwickelt
(Gerlach 2002). Der überwiegende Teil der in
Deutschland gemeldeten Substitutionspatienten wird mit
Methadon behandelt. Aus stereochemischer Sicht handelt
es sich dabei um ein Gemisch (Razemat), das zu gleichen
Teilen aus den beiden Enantiomeren Levomethadon und
Dextromethadon besteht. Die beiden Enantiomere unterscheiden
sich in Bezug auf ihre physikalischen Eigenschaften
nur hinsichtlich der optischen Aktivität (Drehung des
polarisierten Lichts), jedoch sind die pharmakologischen
Unterschiede beträchtlich (Judson et al.1976). Diese Tatsache
ist bereits seit langem bekannt und wurde früh in
die klinisch-experimentelle Beobachtung einbezogen (Kleibel
1963, Ther et al. 1963, Scherbaum et al. 1998).
Das Enantiomer Levomethadon ist die wirksame Substanz,
die mit wesentlich höherer Affinität an den µ-Opiatrezeptoren
bindet und die gewünschte „Substitutionswirkung“
vermittelt. Das Enantiomer Dextromethadon ist zwar auch
pharmakologisch wirksam, wird aber vor allem für unerwünschte
Arzneimittelwirkungen mitverantwortlich gemacht.
Dazu gehören z.B. starkes Schwitzen, gastrointestinale Störungen,
Gewichtszunahme, aber auch lebensbedrohliche
Kammertachykardien und QTc-Verlängerungen.
Die pharmakokinetischen Eigenschaften der beiden Enantiomere
unterscheiden sich ebenfalls, etwa bei der Plasma-
Halbwertzeit und der Verstoffwechselung über verschiedene
P-450-Enzymsysteme (Ferrari et al. 2004, Eap et al. 2002).
Methadon-Razemat ist ausschließlich am Opiat-Rezeptor
schwächer wirksam; im Hinblick auf unerwünschte Wirkungen
und pharmakologische Wechselwirkungen aber von
großer Wichtigkeit (Soyka 2008b).
In Deutschland werden laut Substitutionsregister aktuell
etwa 72.000 Substitutionspatienten behandelt (Bundesministerium
für Gesundheit 2009); die geschätzte Gesamtzahl
aller Opiatabhängigen in Deutschland liegt bei 200.000
bis 250.000. Für die Verwendung der unterschiedlichen
Substanzen zur Substitution gibt es derzeit keine einheitlichen
Richtlinien. Unter Kostenaspekten entwickelte sich
vor Jahren eine starke Ausrichtung auf die Verordnung
von Methadon-Razemat und so ist erklärbar, dass derzeit
noch fast 60% der gemeldeten Patienten mit Methadon-
Razemat behandelt werden (Michels et al. 2009) und nur
etwas mehr als 20% mit Levomethadon (Bundesministerium
für Gesundheit, 2009). Levomethadon wird seit über
20 Jahren für die Substitutionstherapie verwendet und ist
seit 2001 als Fertigarzneimittel in Deutschland verfügbar.
Verschiedene Studien und zahlreiche klinische Befunde aus
der sucht- als auch aus der opioidpflichtigen Schmerztherapie
bescheinigen dem Präparat dabei eine bessere Wirksamkeit
und Verträglichkeit im Vergleich zum Razemat
(Kleibel 1963, Cernaj 2006, Soyka und Zingg 2009, Ulmer
1995).
Für den Einsatz von Levomethadon sprechen auch die Ergebnisse
einer Studie unter dem Gesichtspunkt von Kammertachykardien
(Eap et al. 2007). Die Daten dieser Untersuchung
zeigen, dass Dextromethadon den kardialen
Kaliumkanal um 350% stärker blockiert als Levomethadon
und so das Risiko von QTc-Intervall-Verlängerungen
durch Methadon drastisch erhöht. Dieses Risiko könnte
nach Ansicht der Autoren durch die Verwendung von
Levomethadon vermindert werden. Insbesondere hat auch
die Kombination von Methadon mit Psychopharmaka einen
QTc-verlängernden Effekt, sodass unter dieser Medikation
eine erhöhte Arrhythmiegefahr besteht (Maremmani
et al. 2005, Elsner 2005).
Für eine praxisrelevante Beurteilung der Wirksamkeit und
Verträglichkeit der Substitutionsbehandlung, besonders von
multimorbiden Opiatabhängigen, sind nicht nur die Ergebnisse
aus kontrollierten klinischen Studien wichtig, sondern
vor allem auch die Beobachtungen aus niedergelassenen
Praxen, da sie die realen Alltagsbedingungen abbilden
(Wittchen et al. 2008). So konnte anhand von Daten
einer nicht-interventionellen Beobachtungsstudie auf der
Basis von 1.552 Patienten gezeigt werden, dass während
der Substitution mit Levomethadon signifikant weniger
Beigebrauch, Suchtdruck und Entzugssymptome auftraten
als während der Vorbehandlung mit Methadon-Razemat
(Cernaj 2006).
Im Rahmen der vorliegenden Follow up-Beobachtungsstudie
wird diese Erhebung von Praxisdaten zur Substitutionsbehandlung
mit Levomethadon fortgeführt. Dabei stehen
insbesondere Patienten im Vordergrund, die unter der Vorbehandlung
mit Methadon-Razemat einen instabilen, unbefriedigenden
Behandlungsverlauf aufwiesen, z.B. solche
Patienten mit frühzeitig auftretenden Entzugssymptomen,
hohem Suchtdruck und Beigebrauch sowie verschiedenen
nicht beherrschbaren unerwünschten Arzneimittelwirkungen.
Die Studie wurde mit Unterstützung der Sanofi-
Aventis Deutschland GmbH durchgeführt.
2
MATERIAL UND METHODEN
Die vorliegende Untersuchung ist eine nicht-interventionelle
Beobachtungsstudie bei niedergelassenen Ärzten. Einschlusskriterien
waren
•
Mindestalter 18 Jahre,
•
Opiatabhängigkeit,
•
Substitutionstherapie mit Methadon-Razemat bis unmittelbar
vor Studienbeginn,
•
unbefriedigender Verlauf der Substitutionstherapie.
Zu den Kriterien für eine unbefriedigende Vorbehandlung
gehörten nicht beherrschbare Nebenwirkungen wie übermäßiges
Schwitzen und Magen-Darm-Beschwerden, aber
auch nicht tolerabler Beikonsum und psychische Symptome
wie Depressionen, Psychosen oder anhaltender Sucht-
druck. Bei diesen Patienten wurde nach einer Eingangsuntersuchung
der Verlauf der Substitutionsbehandlung mit
Levomethadon über einen Zeitraum von vier Wochen dokumentiert.
Die Dokumentationsbögen umfassten im Rahmen der Eingangsuntersuchung
neben Patientendaten Angaben zur
Dauer der Opiatabhängigkeit und Informationen zur Substitutionsbehandlung
mit Methadon-Razemat:
•
Beginn,
•
Auftreten von Entzugssymptomen,
•
Suchtdruck und Beigebrauch,
•
Verträglichkeit,
•
Globalbeurteilung.
Begleiterkrankungen und Begleitmedikation wurden dokumentiert
und die Gründe für die Umstellung der Substitutionsbehandlung
auf Levomethadon erfragt.
Nach zwei und vier Wochen wurde neben der Levomethadon-
Dosierung dokumentiert:
•
Auftreten von Entzugssymptomen,
•
Suchtdruck und Beigebrauch,
•
unerwünschte Ereignisse,
•
Beurteilung der Verträglichkeit der Levomethadon-Substitution.
Beim Beobachtungsende wurden darüber hinaus die Fortsetzung
der Levomethadon-Behandlung sowie die Begleittherapie
beschrieben und eine Globalbeurteilung zur bisherigen
Substitution mit Levomethadon abgegeben.
Bei der Eingangsuntersuchung und am Beobachtungsende
wurde ein Drogenscreening durchgeführt. Dazu wurden
Urinproben auf die folgenden Substanzen untersucht: Amphetamin/
Metamphetamin, Barbiturate, Benzodiazepine,
Cannabionoide (THC), Kokain, Opiate (Morphin), LSD
und Alkohol.
Die Daten der Dokumentationsbögen wurden nach Abschluss
der Datenerfassung mit Hilfe des Datenmanagement-
Systems DMSys Version 5.1 erfasst. Dabei wurden
simultane und sequenzielle Plausibilitätskontrollen durchgeführt.
Bei der Kodierung der Klartextangaben kamen
das WHO Drug Dictionary Enhanced 2006 für Begleitmedikationen
und die MedDRA Version 10.0 für Begleiterkrankungen
zum Einsatz.
Alle Daten wurden deskriptiv ausgewertet. Die Beurteilungen
zum Auftreten von Entzugssymptomen, zum Sucht-
druck, zum Beigebrauch und zur Verträglichkeit wurden
in numerische Werte transformiert: nein = 1, wenig = 2,
mäßig = 3, stark = 4, sehr stark = 5. Für diese Daten
wurden mit Hilfe von Wilcoxon-Vorzeichen-Rangtests deskriptive
p-Werte (zweiseitig) berechnet. Die Berechnungen
wurden mit dem Statistikprogrammpaket SPSS for
Windows (Release 15.0.0) durchgeführt.
3
ERGEBNISSE
3.1 PATIENTEN
Die vorliegende statistische Auswertung basiert auf den
Daten von 862 Patienten, die in 87 Zentren von März
2007 bis April 2008 dokumentiert wurden. Die Rekrutierung
der Patienten erfolgte ausschließlich durch niedergelassene
Ärzte. 66,1% (N = 570/862) der Patienten wurden
von Allgemeinmedizinern bzw. praktischen Ärzten,
19,3% (N = 166/862) von Internisten und 8,8% (N = 76/
862) von Ärzten der Fachrichtungen Psychiatrie und Psychotherapie
behandelt. Bei 50 Patienten war die Fachrichtung
des Arztes eine andere oder nicht angegeben.
66,5% (N = 573/862) der Patienten waren Männer. Das
Alter betrug bei den Männern im Median 37,0 Jahre, bei
den Frauen 33,0 Jahre. 39,2% (N = 338/862) der Patien
ten waren verheiratet oder lebten in einer eheähnlichen
Beziehung. 31,8% (N = 274/862) der Patienten hatten Kinder
und 27,0% (N = 233/862) waren berufstätig. Die Patienten
waren im Median seit 13 Jahren opiatabhängig.
Bei 56,3% (N = 485/862) der Patienten bestand die Opiatabhängigkeit
seit 5-20 Jahren (.
Abb. 1).
Abb. 1: Bisherige Dauer der Opiatabhängigkeit (kategorial)
3.1.1 BEGLEITERKRANKUNGEN UND BEGLEITMEDIKATION
Insgesamt wurden bei 78,1% (N = 673/862) der Patienten
Begleiterkrankungen dokumentiert, am häufigsten Hepatitis
C-Infektionen (55,9%; N = 482/862). Unter psychischen
Erkrankungen litten 41,5% (N = 358/862) der Patienten,
darunter 26,6% (N = 229/862) aller Patienten an Depressionen,
14,3% (N = 123/862) an Angstzuständen und
11,0% (N = 95/862) an Persönlichkeitsstörungen. 11,4%
(N = 98/862) der Patienten hatten eine Hepatitis B-Infektion
und 4,4 % (N = 38/862) eine HIV-Infektion (.
Tab. 1).
Tabelle1: Begleiterkrankungen (Mehrfachnennungen möglich)
N %
HIV-Infektion 38 4,41 %
Hepatitis B 98 11,37 %
Hepatitis C 482 55,92 %
Atemwegs- oder sonstige Infektion 62 7,19 %
Magen-Darm-Erkrankung 54 6,26 %
Herz-Kreislauf-Erkrankung 31 3,60 %
Leberinsuffizienz 36 4,18 %
Niereninsuffizienz 5 0,58 %
Psychische Erkrankung 358 41,53 %
Depression 229 26,57 %
Angstzustände 123 14,27 %
Psychose 30 3,48 %
Persönlichkeitsstörung 95 11,02 %
nicht näher spezifiziert 6 0,70 %
Sonstige 84 9,74 %
Gesamt 862 100,00 %
Suchtmed 12 (3) 2010
189
ORIGINALARBEITEN | STABIL-STUDIE: UMSTELLUNG AUF LEVOMETHADON
Trotz des hohen Anteils an Begleiterkrankungen erhielten
nur 40,3% (N = 347/862) der Patienten eine Begleitmedikation.
Dabei wurden Psychopharmaka mit Abstand am
häufigsten gegeben (27,3% der Patienten; N = 235/862).
3.2 BEHANDLUNG
3.2.1 VORTHERAPIE MIT METHADON-RAZEMAT
Die Dauer der Substitutionstherapie mit Methadon-Razemat
vor Umstellung auf Levomethadon betrug im Median
13,0 Monate. Bei 13,6% (N = 117/862) der Patienten erfolgte
die Umstellung innerhalb des ersten Monats nach
Beginn der Substitution mit Methadon-Razemat, bei 33,4%
(N = 288/862) nach mehr als einem Monat bis einem Jahr
und bei 49,8% (N = 429/862) nach mehr als einem Jahr. Bei
3,2% (N = 28/862) der Patienten fehlte hierzu die Angabe.
Die zuletzt gegebene Tagesdosis des Methadon-Razemats
lag im Mittel bei 82,3 ± 41,4 mg (Mittelwert ± Standardabweichung).
26,5% (N = 228/862) der Patienten erhielten
eine Dosierung bis 50 mg, 47,9% (N = 413/862) eine Dosierung
zwischen 50 und 100 mg und 23,8% (N = 205/862)
erhielten mehr als 100 mg Methadon. Bei 1,9% (N = 16/862)
der Patienten fehlte hierzu die Angabe.
Die häufigsten Argumente für eine Umstellung der Substitutionstherapie
von Methadon-Razemat auf Levomethadon
waren eine erwartete bessere Verträglichkeit bei 81,9%
(N = 706/862) der Patienten und eine erwartete bessere bzw.
längere Wirkdauer über 24 Stunden bei 74,2% (N = 640/
862) der Patienten.
3.2.2 LEVOMETHADON
Bei Behandlungsbeginn betrug die mittlere Tagesdosis von
Levomethadon Lösung zur Substitution 51,6 ± 47,2 mg
(Mittelwert ± Standardabweichung). 66,6% (N = 574/862)
der Patienten erhielten eine Dosierung bis 50 mg. 29,2%
(N = 252/862) eine Dosierung über 50-100 mg und 3,5%
(N = 30/862) der Patienten erhielten mehr als 100 mg
Levomethadon (bei 0,7% fehlten die Angaben hierzu). Im
Beobachtungsverlauf kam es nur zu geringfügigen Veränderungen
der Levomethadon-Tagesdosis. Der Median der
Tagesdosis lag bei allen drei Untersuchungszeitpunkten
bei 45,0 mg.
Die dokumentierte Behandlungsdauer mit Levomethadon
lag im Median bei 31,0 Tagen. Bei 94,4% (N = 814/862)
der Patienten wurde die Substitution mit Levomethadon
über das Beobachtungsende hinaus fortgesetzt. Bei 4,6%
(N = 40/862) erfolgte ein Abbruch der Behandlung und
für 0,9% (N = 8/862) lagen keine Angaben zur Weiterbehandlung
vor. Bei den 40 Patienten mit einem vorzeitigen
Ende der Behandlung waren die am häufigsten genannten
Gründe dafür „Patient nicht mehr erschienen“ (1,6% der
Patienten; N = 14/862), „ungenügende Wirksamkeit“ (1,3%;
N = 11/862) und „Patientenwunsch“ (0,8%; N = 7/862).
3.3 WIRKSAMKEIT
3.3.1 DROGENSCREENING UND BEIGEBRAUCH
Sowohl bei der Eingangsuntersuchung als auch am Beobachtungsende
wurde ein Drogenscreening für alle wichtigen
psychotropen Substanzen (Amphetamin/Metamphetamin,
Barbiturate, Benzodiazepine, Cannabinoide (THC),
Kokain, Opiate (Morphin), LSD und Alkohol) durchgeführt.
Das Drogenscreening bei der Eingangsuntersuchung spiegelt
aufgrund der Substitution mit Methadon-Razemat bis
zu diesem Zeitpunkt den Beigebrauch unter Methadon-
Razemat wieder: Bei 73,5% (N = 634/862) der Patienten
fand sich mindestens ein positiver Drogennachweis, bei
22,4% (N = 193/862) der Patienten wurden keine der unter-
Abb. 2:
Anteil positiver Drogenscreening-Befunde bei
der Eingangsuntersuchung (Methadon-Razemat)
und am Beobachtungsende (Levomethadon)
190 Suchtmed 12 (3) 2010
STABIL-STUDIE: UMSTELLUNG AUF LEVOMETHADON | ORIGINALARBEITEN
suchten Drogen nachgewiesen. Bei 4,1% (N = 35/862)
der Patienten war kein Drogenscreening angegeben.
Das Drogenscreening am Beobachtungsende spiegelt den
Beigebrauch unter der Therapie mit Levomethadon wider:
Bei 44,1% (N = 380/862) der Patienten fand sich mindestens
ein positiver Drogennachweis, bei 49,1% (N = 423/
862) der Patienten wurden keine der untersuchten Drogen
nachgewiesen und bei 6,8% (N = 59/862) der Patienten war
kein Drogenscreening angegeben.
Die Untersuchungshäufigkeit der einzelnen Drogenarten
war sehr unterschiedlich. Es wurde am häufigsten versucht,
den Beigebrauch von Opiaten, Benzodiazepinen und Kokain
nachzuweisen bzw. auszuschließen (.
Abb. 2):
Opiate wurden unter Methadon-Razemat bei 95,1% (N =
820/862) und unter Levomethadon bei 92,1% (N = 794/
862) der Patienten untersucht. Ein positiver Nachweis fand
sich bei 43,3% (N = 355/820) der untersuchten Patienten
unter Methadon-Razemat, unter Levomethadon dagegen
nur noch bei 10,3% (N = 82/794) der Patienten.
Benzodiazepine wurden unter Methadon-Razemat bei 94,9%
(N = 818/862) und unter Levomethadon bei 92,7% (N =
799/862) der Patienten untersucht. Ein positiver Nachweis
fand sich bei 45,0% (N = 368/818) der untersuchten Patienten
unter Methadon-Razemat, unter Levomethadon dagegen
nur noch bei 22,2% (N = 177/799) der Patienten.
Kokain wurde unter Methadon-Razemat bei 93,4% (N =
805/862) und unter Levomethadon bei 90,5% (N = 780/862)
der Patienten untersucht. Ein positiver Nachweis fand sich
bei 15,8% (N = 127/805) der untersuchten Patienten unter
Methadon-Razemat, unter Levomethadon dagegen nur noch
bei 4,0% (N = 31/780) der Patienten.
Zusätzlich zum erhobenen Drogenscreening wurden die
beteiligten Ärzte auch direkt nach dem Beikonsum ihrer
Patienten gefragt. Der Anteil an Patienten ohne Beikonsum
war unter der Substitutionstherapie mit Levomethadon
deutlich höher (57,0%; N = 491/862) als unter der Thera
pie mit Methadon-Razemat (17,4%; N = 150/862).
3.3.2 AUFTRETEN VON ENTZUGSSYMPTOMEN
Das Auftreten von Entzugssymptomen wurde von den behandelnden
Ärzten im Rahmen der Eingangsuntersuchung
sowie am Beobachtungsende beurteilt. Bei der Eingangsuntersuchung
wurden dabei die Entzugssymptome unter
dem Einfluss der Vortherapie mit Methadon-Razemat beurteilt.
Am Beobachtungsende sollte das Auftreten der Entzugssymptome
unmittelbar vor der nächsten Gabe von
Levomethadon eingeschätzt werden.
Das frühzeitige Auftreten von Entzugssymptomen innerhalb
der letzten 24 Stunden vor der nächsten Substitution
wurde mithilfe der Kategorien „nein“, „wenig“, „mäßig“,
„stark“ und „sehr stark“ beurteilt. Der Anteil der Patienten
ohne ein frühzeitiges Auftreten von Entzugssymptomen
erhöhte sich deutlich im Beobachtungsverlauf: Während
vor der Umstellung der Substitutionstherapie auf Levomethadon
14,4% (N = 124/862) der Patienten frei von Entzugssymptomen
waren, betrug der Anteil bei Beobachtungsende
58,6% (N = 505/862). Bezogen auf die Patienten mit
validen Angaben zur Eingangsuntersuchung und bei Beobachtungsende
(N = 751) betrug die Verbesserung im Mittel
1,45 Kategorienstufen (p < ,001).
Das Auftreten sowie die Ausprägung der Entzugssymptome
Schwitzen, innere Unruhe, Tachykardie, Unkonzentriertheit
und Angstzustände wurde ebenfalls mit Hilfe der Kategorien
„nein“, „wenig“, „mäßig“, „stark“ und „sehr stark“
beurteilt. Die folgende Tabelle 2 stellt den Anteil der Patienten
ohne diese Entzugssymptome bei der Eingangsuntersuchung
sowie am Beobachtungsende dar (.
Tab. 2).
Die Daten zeigen bei allen beurteilten Symptomen einen
höheren Anteil an Patienten, die unter dem Einfluss von
Levomethadon am Beobachtungsende frei von Entzugssymptomen
waren gegenüber der Eingangsuntersuchung.
Die Veränderungen der Beurteilungen sind für alle erfragten
Entzugssymptome statistisch signifikant (p < ,001).
Eingangsuntersuchung
(Methadon Razemat)
Beobachtungsende
(Levomethadon)
Signifikanz*
(Wilcoxon Rang-Test,
zweiseitig)
Schwitzen 9,4 % (N = 81) 40,8 % (N = 352) p <,001
Innere Unruhe 12,6 % (N = 109) 47,2 % (N = 407) p <,001
Tachykardie 38,9 % (N = 335) 72,3 % (N = 623) p <,001
Unkonzentriertheit 17,4 % (N = 150) 49,8 % (N = 429) p <,001
Angstzustände 31,9 % (N = 275) 60,4 % (N = 521) p <,001
* Bezogen auf die Veränderung der kategorialen Einschätzung
Tabelle 2: Anteil der Patienten ohne Entzugssymptome (N = 862)
Suchtmed 12 (3) 2010 191
3.3.3 SUCHTDRUCK
Der Anteil der Patienten ohne Suchtdruck (Craving) erhöhte
sich deutlich im Beobachtungsverlauf. Während vor einer
Umstellung der Substitutionstherapie auf Levomethadon
11,8% (N = 102/862) der Patienten frei von diesem Symptom
waren, betrug der Anteil bei Beobachtungsende 57,7%
(N = 497) (.
Abb. 3). Bezogen auf die Patienten mit validen
Angaben zur Eingangsuntersuchung und bei Beobachtungsende
(N = 829) betrug die Verbesserung im Mittel
1,4 Kategorienstufen (p < ,001) (.
Abb. 3).
3.4 VERTRÄGLICHKEIT
Sowohl im Rahmen der Eingangsuntersuchung als auch
am Beobachtungsende wurden von den behandelnden Ärzten
die folgenden Unverträglichkeitsreaktionen beurteilt:
Schwitzen, Kopfschmerzen, Magen-Darm-Probleme, Schlafstörungen,
Müdigkeit/Sedierung, Stimmungsstörungen/
Abb. 3:
Patienten ohne Suchtdruck
(p < ,001; zweiseitiger Wilcoxon Rang-Test)
psychische Probleme, Libidostörungen, Antriebslosigkeit
und Schmerzen. Das Auftreten sowie die Ausprägung der
Reaktionen wurde mit Hilfe der Kategorien „nein“, „wenig“,
„mäßig“, „stark“ und „sehr stark“ beurteilt.
Die Daten zeigen bei allen beurteilten Unverträglichkeitsreaktionen
einen höheren Anteil an Patienten ohne diese Reaktionen
am Beobachtungsende (d.h. unter dem Einfluss
von Levomethadon) gegenüber der Eingangsuntersuchung
(d.h. unter dem Einfluss von Methadon-Razemat). Die Veränderungen
der Beurteilungen sind für alle erfragten Reaktionen
statistisch signifikant (p < ,001).
.
Tabelle 3 stellt den Anteil der Patienten ohne diese Unverträglichkeitsreaktionen
(Einschätzung „nein“) bei der
Eingangsuntersuchung sowie am Beobachtungsende dar.
UNERWÜNSCHTE ARZNEIMITTELWIRKUNGEN
Bei sieben der 862 Patienten (0,81%) traten insgesamt 13
unerwünschte Arzneimittelwirkungen (UAW) auf. Sie be-
Eingangsuntersuchng
(Methadon-Razemat)
Beobachtungsende
(Levomethadon)
Signifikanz*
(Wilcoxon Rang Test,
zweiseitig)
Schwitzen 8,1 % (N = 70) 40,0 % (N = 345) p <,001
Kopfschmerzen 46,9 % (N = 404) 80,5 % (N = 694) p <,001
Magen-Darm-Probleme 29,6 % (N = 255) 66,0 % (N = 569) p <,001
Schlafstörungen 13,5 % (N = 116) 43,0 % (N = 371) p <,001
Müdigkeit / Sedierung 22,5 % (N = 194) 57,8 % (N = 498) p <,001
Stimmungsstörungen /
psychische Probleme
17,2 % (N = 148) 48,5 % (N = 418) p <,001
Libidostörungen 36,4 % (N = 314) 59,4 % (N = 512) p <,001
Antriebslosigkeit 20,3 % (N = 175) 55,0 % (N = 474) p <,001
Schmerzen 59,9 % (N = 516) 83,1 % (N = 716) p <,001
* Bezogen auf die Veränderung der kategorialen Einschätzung
trafen am häufigsten die MedDRA Primary System Organ
Class „Gastrointestinal disorders“ (0,46% der Patienten).
Die häufigsten Einzelnennungen gemäß MedDRA Preferred
Term waren Verstopfung (N = 2; 0,23%) sowie Ekzeme,
allergische Hautreaktionen, Schwindel, Gastritis, gastrointestinale
Blutungen, Kopfschmerzen, Schwitzen, Unwohlsein,
Übelkeit, Ödeme und Erbrechen (jeweils N = 1;
0,12%). Schwerwiegende unerwünschte Arzneimittelwirkungen
traten nicht auf. Ein Patient verstarb aufgrund eines
Leberversagens im Verlauf der Studie (0,12% aller
Patienten). Ein Kausalzusammenhang mit Levomethadon
konnte ausgeschlossen werden.
3.5 GLOBALBEURTEILUNG DER SUBSTITUTIONSTHERAPIE
Die nachfolgenden Abbildungen/Tabellen enthalten die Beurteilung
der Substitutionstherapie mit Levomethadon nach
ca. vier Wochen bzw. bei Beobachtungsende sowie – zum
Vergleich – die Beurteilung der Therapie mit einem Methadon-
Razemat bei der Eingangsuntersuchung.
3.5.1 WIRKSAMKEIT
Die Wirksamkeit der Substitutionstherapie mit Levomethadon
wurde bei 91,9% (N = 792/862) der Patienten mit
„sehr gut“ bis „gut“ und bei 5,1% (N = 44/862) mit „mäßig“
bis „unbefriedigend“ angegeben (fehlende Angaben:
3,0%) (.
Abb. 4). Die Wirksamkeit der Behandlung mit
einem Methadon-Razemat vor Therapieumstellung auf
Levomethadon wurde bei 28,0% (N = 241/862) der Patienten
mit „sehr gut“ bis „gut“ und bei 71,3% (N = 615/862)
mit „mäßig“ bis „unbefriedigend“ angegeben (fehlende
Angaben: 0,7%. Bezogen auf die Patienten mit validen
Angaben zur Eingangsuntersuchung und bei Beobachtungsende
(N = 830) betrug der Unterschied im Mittel 1,2
Kategorienstufen zu Gunsten von Levomethadon und war
statistisch signifikant (p < ,001).
Abb. 4: Globalbeurteilung der Wirksamkeit der Substitutionstherapie
mit Levomethadon
3.5.2 VERTRÄGLICHKEIT
Die Verträglichkeit der Substitutionstherapie mit Levomethadon
wurde bei 93,4% (N = 805/862) der Patienten mit
„sehr gut“ bis „gut“ und bei 3,5% (N = 30/862) mit „mäßig“
bis „unbefriedigend“ angegeben (fehlende Angaben:
3,1%). Die Verträglichkeit der Behandlung mit einem Methadon-
Razemat vor Therapieumstellung wurde bei 23,0%
(N = 198/862) der Patienten mit „sehr gut“ bis „gut“ und
bei 76,2% (N = 657/862) mit „mäßig“ bis „unbefriedigend“
angegeben (fehlende Angaben: 0,8%). Der Unterschied
betrug im Mittel 1,4 Kategorienstufen zu Gunsten
von Levomethadon und war statistisch signifikant (p < ,001;
N = 828).
3.5.3 COMPLIANCE
Die Patienten-Compliance unter der Substitutionstherapie
mit Levomethadon wurde bei 87,2% (N = 752/862) der
Patienten mit „sehr gut“ bis „gut“ und bei 9,6% (N = 83/
862) mit „mäßig“ bis „unbefriedigend“ angegeben (fehlende
Angaben: 3,1%). Die Patienten-Compliance unter der
Behandlung mit einem Methadon-Razemat vor Therapieumstellung
wurde bei 49,9% (N = 430/862) der Patienten
mit „sehr gut“ bis „gut“ und bei 49,0% (N = 422/862) mit
„mäßig“ bis „unbefriedigend“ angegeben (fehlende Angaben:
1,2%). Der Unterschied betrug dabei im Mittel 0,80
Kategorienstufen zugunsten von Levomethadon und war
statistisch signifikant (p < ,001; N = 825) (.
Tab. 4).
Tabelle 4: Globalbeurteilung zur Compliance der Patienten
Eingangs Beobachtungsuntersuchung
ende
(Methadon(
Levo-
Razemat) methadon)
N % N %
sehr gut 76 8,8 % 331 38,4 %
gut 354 41,1 % 421 48,8 %
mäßig 323 37,5 % 74 8,6 %
unbefriedigend 99 11,5 % 9 1,0 %
keine Angabe 10 1,2 % 27 3,1 %
Total 862 100 % 862 100 %
3.5.4 BEFINDLICHKEIT
Die Befindlichkeit des Patienten wurde unter der Substitutionstherapie
mit Levomethadon bei 88,4% (N = 762/862)
der Patienten mit „sehr gut“ bis „gut“ und bei 8,5% (N =
73/862) mit „mäßig“ bis „unbefriedigend“ angegeben (feh-
lende Angaben: 3,1%). Die Befindlichkeit des Patienten un-862) der Patienten als „gleich“ und bei 0,9% (N = 8/862)
ter der Behandlung mit einem Methadon-Razemat vor The-der Patienten als „schlechter“ bzw. „viel schlechter“ berapieumstellung
wurde bei 18,2% (N = 157/862) der Patien-wertet (bei 2,9% fehlte diese Angabe) (.
Abb. 6).
ten mit „sehr gut“ bis „gut“ und bei 80,9% (N = 697/862)
mit „mäßig“ bis „unbefriedigend“ angegeben (fehlende
Angaben: 0,9%). Der Unterschied betrug dabei im Mittel
1,25 Kategorienstufen zu Gunsten von Levomethadon und
war statistisch signifikant (p < ,001; N = 827) (.
Tab. 5).
Eingangs
untersuchung
(Methadon-
Razemat)
Beobachtungs
ende
(Levo
methadon)
N % N %
sehr gut 10 1,2 % 238 27,6 %
gut 147 17,1 % 524 60,8 %
mäßig 480 55,7 % 66 7,7 %
unbefriedigend 217 25,2 % 7 0,8 %
keine Angabe 8 0,9 % 27 3,1 %
Total 862 100 % 862 100 %
Tabelle 5: Globalbeurteilung zur Befindlichkeit der Patienten
3.5.5 VERGLEICH ZUR VORTHERAPIE
Die Wirksamkeit der Substitutionstherapie mit Levomethadon
wurde im Vergleich zur Vortherapie mit einem Methadon-
Razemat bei 82,3% (N = 709/862) der Patienten mit
„viel besser“ bzw. „besser“, bei 13,9% (N = 120/862) der
Patienten als „gleich“ und bei 0,9% (N = 8/862) der Patienten
als „schlechter“ bewertet (bei 2,9% fehlte diese Angabe)
(.
Abb. 5).
Die Verträglichkeit der Substitutionstherapie mit Levomethadon
wurde im Vergleich zur Vortherapie mit einem
Methadon-Razemat bei 85,7% (N = 739/862) der Patienten
mit „viel besser“ bzw. „besser“, bei 10,4% (N = 90/
Abb. 5: Beurteilung der Wirksamkeit der Substitutionstherapie mitLevomethadon im Vergleich zur Vortherapie mit Methadon-Razemat
Abb. 6: Beurteilung der Verträglichkeit der Substitutionstherapie mitLevomethadon im Vergleich zur Vortherapie mit Methadon-Razemat
4 DISKUSSION
Nach den Richtlinien der Bundesärztekammer verläuft die
Behandlung von opiatabhängigen Patienten – im Rahmen
eines umfassenden Therapiekonzeptes – in verschiedenen
Stufen und hängt stark von der individuellen Disposition
des Opiatabhängigen ab (Richtlinien der Bundesärztekammer
2002). Die zur Verfügung stehenden Substitutionsmittel
können dabei je nach Situation des Patienten zum Einsatz
kommen (Michels et al. 2009).
Pharmakologische Daten aus in vitro- und in vivo-Untersuchungen
zur stereoselektiven Verstoffwechselung lieferten
in der Vergangenheit bereits wichtige Hinweise zum differenzierten
Einsatz von Levomethadon und Methadon-Razemat.
Spätestens seit den Untersuchungen von Eap et al.
2007 sind die pharmakologischen Zusammenhänge zwischen
dem Enantiomer Dextromethadon, der genetisch festgelegten
Fähigkeit zur Methadon-Metabolisierung durch
das Cytochrom P450-Enzymsystem CPY2B6 und der Erhöhung
des Risikos für schwere kardiale Arrhythmien und
den plötzlichen Herztod deutlich. Das im Methadon-Razemat
enthaltende Enantiomer Dextromethadon wird
stereoselektiv über CYP2B6 metabolisiert und besitzt durch
Blockade der sog. kardialen hERG-Kanäle ein 350% höheres
Kardiotoxizitäts-Potenzial als Levomethadon. Da
mindestens 6% aller opiatabhängigen Patienten einen
CPY2B6-Defekt aufweisen, ist dieser Genotyp für die Praxis
von hoher Relevanz. Durch weitere Risikofaktoren wie
Hypokaliämie, Hypocalciämie, hohe Arzneimittelkonzentrationen
und pharmakokinetische Wechselwirkungen kann
die Dextromethadon-Konzentration im Blut deutlich ansteigen,
so dass das Auftreten von Torsade de pointes signifikant
erhöht wird (Elsner 2005, Soyka 2008a und b).
Da die therapeutische Aktivität allein von Levomethadon
vermittelt wird, führt die Umstellung der Patienten von
Methadon auf Levomethadon zu einer Halbierung der Substanzmenge
und zu einer daraus resultierenden Senkung
der Plasmakonzentrationen, wodurch die opioidbedingte
Toxizität und Nebenwirkungsrate deutlich gesenkt werden
kann (Soyka 2008a und b). Da es aber auch hier noch keine
evidenzbasierten Richtlinien gibt, sind empirische Anhaltspunkte
für die Praxis von übergeordneter Bedeutung.
Vor diesem Hintergrund kommt den Ein- und Ausschlusskriterien
bei Studien zur Substitutionstherapie eine besonders
wichtige Rolle zu und sie werden kontrovers diskutiert
(u.a. bei Wittchen et al. 2009). Zum einen ist es durch
die hohe Komorbiditätsrate oft schwierig zu entscheiden,
welche Einflüsse die einzelnen Faktoren auf den Allgemein-
zustand haben. Viele klinische Studien schließen daher
multimorbide Patienten aus, nur stabile und unauffällige
Patienten dürfen rekrutiert werden. Dadurch wird die resultierende
Stichprobe aber oft stark reduziert, was die Relevanz
der Studienergebnisse erheblich beeinträchtigt. Zudem
muss ein hoher Prozentsatz der opiatabhängigen Patienten
tatsächlich als multimorbid eingestuft werden. Dadurch
sind Studien, die sich an den Praxisgegebenheiten
orientieren und die auch diese Klientel repräsentieren, für
den behandelnden Arzt von höherer Relevanz. Das ist bei
den vorliegenden Daten der Fall, die ausnahmslos in niedergelassenen
Praxen erhoben wurden. Sie können dadurch
die Behandlungsverläufe in der ärztlichen Alltagsroutine
weitgehend abbilden.
Die vorliegende Untersuchung beleuchtet die Umstellung
der Substitutionsbehandlung von Methadon-Razemat auf
Levomethadon. Das Kollektiv umfasst 862 opiatabhängige
Patienten, die aufgrund einer unbefriedigenden Substitution
mit Methadon-Razemat auf Levomethadon umgestellt
wurden. Gründe für die Umstellung auf Levomethadon
konnten u.a. erhöhter Suchtdruck, nicht tolerabler Beikonsum
oder nicht beherrschbare Nebenwirkungen der Vortherapie
sein. Bemerkenswert ist dabei, dass das Patientenklientel
mehrheitlich bereits lange drogenabhängig war
(im Median 13 Jahre) und eine hohe Multimorbiditätsrate
aufwies. So litten 78,1% aller Patienten an mindestens
einer Begleiterkrankung, wobei der größte Anteil auf eine
Hepatitis C-Infektion entfiel (55,9%).
Die Ergebnisse dieser Beobachtungsstudie zeigen nach der
Umstellung der Substitutionsbehandlung von Methadon-
Razemat auf Levomethadon eine deutliche Verbesserung
der Wirksamkeit und Verträglichkeit sowie eine signifikante
Verringerung des Suchtdrucks und des Beigebrauchs. Im
Vergleich zur Vortherapie wurden unter der Behandlung
mit Levomethadon bei deutlich weniger Patienten Entzugssymptome
dokumentiert. Durch die Substitutionsbehandlung
bedingte Unverträglichkeiten wie Schwitzen, Kopf
schmerzen, Magen-Darm-Probleme, Schlafstörungen, Müdigkeit/
Sedierung, Stimmungsstörungen/psychische Probleme,
Libidostörungen, Antriebslosigkeit und Schmerzen wurden
im Vergleich zur Vortherapie unter der Behandlung mit
Levomethadon ebenfalls signifikant seltener dokumentiert.
Die Daten bestätigen die Ergebnisse einer Beobachtungsstudie
mit 1.552 Patienten (Cernaj 2006), bei denen ebenfalls
die Umstellung von Methadon-Razemat auf Levomethadon
dokumentiert wurde. Im Gegensatz zu dieser Untersuchung
wurde bei der vorliegenden Studie vorausgesetzt, dass die
Vorbehandlung mit Methadon-Razemat nach Einschätzung
des Arztes unbefriedigend verlief. Vor diesem Hintergrund
waren auch die aktuellen Ergebnisse z.B. in Bezug auf
Beigebrauch, Entzugssymptomatik und Suchtdruck im Vergleich
der Studien für die Methadon-Vorbehandlung noch
ungünstiger. Die Ausgangsbedingungen für einen positiven
Therapieverlauf nach Umstellung auf Levomethadon
waren somit deutlich schlechter.
Zum Beispiel war der Anteil von Patienten mit einem nachgewiesenen
Beigebrauch in den aktuellen Daten mit 73,5%
höher als der in der Literatur berichtete Anteil von 61,2%
(Cernaj 2006). Nach der Umstellung auf Levomethadon
war der Unterschied jedoch geringer: Während von einem
positiven Drogennachweis in der vorhergehenden Studie
bei 39,8% der Patienten berichtet wurde, beträgt der Anteil
in den vorliegenden Daten 44,1%. Die Ergebnisse zeigen
damit, dass auch Patienten mit unbefriedigendem Therapieverlauf
unter Methadon durchaus von einer Substitution
profitieren können, wenn sie entsprechend umgestellt
werden.
Diese Ergebnisse stehen in einem gewissen Widerspruch
zu denen von Verthein et al. (2007), die in einer doppelblinden
Studie bei stabil auf ein Substitutionsmittel eingestellten
Patienten keine Effekte bei der Umstellung beobachten
konnten. Untersuchte Merkmale waren in diesem Fall
psychische Befindlichkeit, depressive Verstimmungen, Ängstlichkeit,
Suchtdruck und Beigebrauch. Obwohl die kleine
Zahl von Patienten (n = 68) die Aussagekraft der Studie
ohnehin relativiert, dürfte der Unterschied zu weiten Teilen
eher auf die stark differierenden Ein- und Ausschlusskriterien
zurückzuführen sein.
Das Patientenkollektiv von Wittchen et al. (2009) ist durch
hohe Belastung mit somatischen und mentalen Krankheiten
als multimorbid charakterisiert. Die Autoren konnten
den hohen Nutzen der Substitutionstherapie für diese Gruppe
klar belegen und betonen mehrfach die hohe Praxisrelevanz,
da die in ihrer Studie gewählten Bedingungen im
niedergelassenen Bereich regelmäßig anzutreffen sind.
Die vorliegende STABIL-Studie wurde mit einem vergleichbaren
Patientenkollektiv durchgeführt, was die durchschnittliche
Dauer der Krankheit und des körperlichen und men-
talen Gesamtstatus betrifft. Die Ergebnisse untermauern
die bereits in verschiedenen pharmakokinetischen Untersuchungen
erhobenen Hinweise, dass die opioidbedingte
Toxizität und die Nebenwirkungsrate durch Umstellung der
Patienten von Methadon auf Levomethadon deutlich gesenkt
werden können. Wirksamkeit und Verträglichkeit der
Therapie werden signifikant verbessert, so dass Patienten,
die zuvor mit Methadon-Razemat nur unbefriedigend behandelt
werden konnten, deutlich von einer Umstellung
profitieren.
5 LITERATUR
Bundesministerium für Gesundheit (2009): Drogen- und Suchtbericht
2008, Referat für Öffentlichkeitsarbeit des Bundesministeriums für
Gesundheit und soziale Sicherung. Eigenverlag, Berlin
Cernaj J (2006): Levomethadon signifikant besser als Methadon. Praxis-
Depesche 23, 1-4
Eap CB, Buclin T, Baumann P (2002): Interindividual Variability of the
Clinical Pharmacokinetics of Methadone. Clin Pharmacokinet 41
(14),1153-1193
Eap CB et al. (2007): Stereoselective block of hERG channel by (S)methadone
and QT interval prolongation in CYP2B6 slow metabolizers.
Clin Pharmacol Ther 81 (5), 719-728
Elsner H (2005): Kammertachykardien („Torsade de Pointes“) und weitere
Herzrhythmusstörungen unter Methadonsubtitution: Risikominderung
durch Medikamentenumstellung. Suchtmed 7 (4), 257263
Ferrari A, Coccia CPR, Bertolini A, Sternieri E (2004): Methadone –
metabolism, pharmacokinetics and interactions; Pharmacol Res 50,
551-559
Gerlach R (2002): Drug-substitution treatment in Germany: a critical
overview of its history, legislation, and current practice. J Drug Issues
32 (2), 503-521
Judson BA, Horns WH, Goldstein A (1976): Side effects of levomethadone
and racemic methadone in a maintenance program. Clin Pharmacol
Ther 20 (4), 445-449
Kleibel F (1963): Klinisch-experimentelle Untersuchungen eines neuen
linksdrehenden Polamidonpräparates (Levomethadon). Med Welt 31,
1573-1575
Maremmani I et al. (2005): QTc interval prolongation in patients on long
term methadone maintenance therapy. Eur Addict Res 11, 44-49
Michels I, Sander G, Stöver H (2009): Praxis, Probleme und Perspektiven
der Substitutionsbehandlung Opioidabhängiger in Deutschland.
Bundesgesundheitsblatt – Gesundheitsforschung – Gesundheitsschutz
52, 111-121
Richtlinien der Bundesärztekammer zur Durchführung der substitutionsgestützten
Behandlung Opiatabhängiger. Dtsch Ärzteblatt (2002)
99 (21) A 1458-A 1461
Scherbaum N, Finkbeiner T, Leifert K, Gastpar M (1998): The efficacy of lmethadone
and racemic methadone in substitution treatment for
opiate addicts – a double blind comparison; Pharmacopsychiat 29,
212-215
Shriniwas G et al.(1992): Bioequivalence of Racemic Drugs. J Clin
Pharmacol 32, 935-943
Soyka M (2008a): Sicherheitsaspekte in der Methadonsubstitution – Teil
2: Klinisch-pharmakologische Aspekte. Suchtmed 10 (2), 119-144
Soyka M (2008b): Sicherheitsaspekte in der Methadonsubstitution – Teil
1: Rechtliche Rahmenbedingungen, Mortalität, aktuelle Ergebnisse
der Therapieforschung. Suchtmed 10 (1), 7 – 27
Soyka M, Zingg C (2009): Feasabilitity and safety of transfer from racemic
methadone to (R)-methadone in primary care: Clinical results from a
open study. World J Biol Psych 10 (3), 217-224
Ther L, Lindner E, Vogel C (1963): Zur pharmakologischen Wirkung der
optischen Isomeren des Methadons; Dtsch Apothekerzeitung 17,
514-520
Ulmer A (1995): Klinische Auffälligkeiten bei der Umstellung von Levomethadon
auf Methadon-Razemat. Der Kassenarzt 12, 49-50
Verthein U, Reimer J, Ullmann R und Haasen C (2007): Psychische Befindlichkeit
in der Substitutionsbehandlung mit Levomethadon und d-l-
Methadon – eine doppelt randomisierte cross-over-Studie. Sucht 53
(1), 32-41
Wittchen HU et al. (2008): Feasibility and outcome of substitution
treatment of heroin-dependent patients in specialized substitution
centers and primary care facilities in Germany: A naturalistic study in
2694 patients. Drug and Alcohol Depend 95(3), 245-257
Auch als File fuer bessere Graphiken:metha auf pola
Orginalquelle ist: http://www.ecomed-medizin.de/sj/sfp/abstract/ArtikelId/11160
Substitution in der EU heute weit verbreitet
Die Substitutionstherapie bei
problematischen Drogenkonsumenten ist
in der Europäischen Union (EU) heute
weit verbreitet. Erste Versuche –
hauptsächlich mit Methadon – begannen
Ende der 60er-Jahre, vor allem in
Nordeuropa. Bis Mitte der 90er-Jahre
war die Drogensubstitution in allen
EU-Mitgliedstaaten umgesetzt worden.
Europaweit herrscht heute überwiegend
Konsens bezüglich des Nutzens dieser
Therapieform. Dennoch ist sie in einigen
Ländern nach wie vor ein heikles Thema.
Wissenschaftliche Nachweise lassen
darauf schließen, dass mithilfe der
Substitutionstherapie Kriminalität,
Infektionskrankheiten und
drogenbedingte Todesfälle reduziert und
das körperliche, seelische und soziale
Wohlbefinden von abhängigen
Drogenkonsumenten verbessert werden
können. Als Gegenargument wird jedoch
angeführt, sie biete keine Heilung,
sondern sei lediglich eine halbherzige
Maßnahme, die das Problem des
Drogenkonsums nicht tatsächlich löse.
Die EBDD ist der Auffassung, dass sich die
politische Debatte über dieses Thema
nicht nur auf die Vor- und Nachteile
erstrecken sollte.
Die Substitutionstherapie
sollte vielmehr als ein Element innerhalb
eines ganzen Bündels von Maßnahmen
gegen das Problem des Drogenkonsums
gesehen werden, zu dem auch die
drogenfreie Therapie zählt.
Schätzungen zufolge erhalten
weltweit ungefähr eine halbe
Million Drogenkonsumenten eine
Substitutionstherapie. Davon
befinden sich mehr als 300 000 in
Europa und schätzungsweise
110 000 in den USA [1].
Methadon ist immer noch die am
häufigsten verwendete Substanz, obwohl
sie längst nicht mehr die Einzige ist.
In Frankreich ist Buprenorphin
vorherrschend. Andere EU-Mitgliedstaaten
haben Versuche mit Substanzen wie
Dihydrocodein, Morphin mit verzögerter
Wirkung und Levo-Alpha-Acetyl-Methadol
(LAAM) durchgeführt. Auf Empfehlung
der Europäischen Agentur für die
Beurteilung von Arzneimitteln (EMEA)
wird LAAM aufgrund des Auftretens von
lebensbedrohlichen Herz-Kreislauf-
Erkrankungen unter den in LAAM-
Therapie befindlichen Personen nun
jedoch nicht mehr eingesetzt.
Die Verwendung von Heroin bei
stabilisierten chronischen
Opiatkonsumenten wird seit 1997 in den
Niederlanden und seit kurzem auch in
Deutschland untersucht und ist in
anderen Mitgliedstaaten im Gespräch.
Im Vereinigten Königreich wird Heroin
selektiv in kleinem Umfang schon seit
einigen Jahrzehnten verschrieben.
Fakten, Zahlen und Untersuchungen sind
natürlich Voraussetzung für eine rationale
Erörterung dieser Thematik.
Bis vor kurzem waren aktuelle Daten auf
EU-Ebene über die Evaluation und
Qualität von Substitutionstherapien
Mangelware.
Dann veröffentlichte die EBDD Ende 2000
in ihrer Reihe Insights: Reviewing current
practice in drug-substitution treatment in
the European Union [1] jedoch einen
umfassenden Überblick über die jüngste
Praxis der Drogensubstitution.
Definition:
Die Substitutionstherapie ist eine Form der medizinischen
Fürsorge für Opiatabhängige (insbesondere Heroinabhängige), die auf der
Verabreichung einer Substanz beruht, die der bislang eingenommenen Droge
ähnlich oder mit ihr identisch ist. Sie wird in zwei Formen durchgeführt: als
Erhaltungstherapie – durch Verabreichung einer ausreichenden Dosis zur
Vermeidung des Risikoverhaltens bzw. gesundheitsschädigenden Verhaltens –
und als Entgiftung – durch stufenweise Herabsetzung der Dosis bis auf null.
Die Therapie kann mit oder ohne psychosoziale Unterstützung erfolgen.
Wichtige politische Themen auf einen Blick
1. Die Substitutionstherapie ist wesentlicher Bestandteil eines umfassenden
Ansatzes zur Drogentherapie. Sie kann dazu beitragen, das Risiko einer
HIV-Infektion oder Überdosis zu reduzieren und den Konsum legaler und
illegaler Drogen und die drogenbedingte Kriminalität zu verringern.
2. Es spricht einiges dafür, die Substitutionstherapie durch psychosoziale Fürsorge
zu unterstützen. In der Praxis fehlen diese Programme jedoch häufig, und der
Schwerpunkt liegt mehr auf der Substitution als auf der Therapie.
3. Die derzeit verwendeten Substanzen sind u. a. Methadon, Buprenorphin,
Dihydrocodein, Morphin mit verzögerter Wirkung und Heroin. In nahezu allen
EU-Mitgliedstaaten ist eine Substanz vorherrschend. Insgesamt wird
Methadon am häufigsten eingesetzt. Um optimale Ergebnisse zu erzielen,
sollte sowohl die Auswahl der Substanz als auch deren Dosierung auf den
jeweiligen Betroffenen abgestimmt werden.
4. Der Zugang zur Substitutionstherapie ist in der EU sehr unterschiedlich.
Einige Länder und Programme beschränken den Zugang anhand strenger
Kriterien („hochschwelliger“ Zugang). Andere fordern als einzige
Zugangsvoraussetzung die Opiatabhängigkeit („niedrigschwelliger“ Zugang).
5. In den meisten EU-Ländern wird die Substitutionstherapie entweder von
praktischen Ärzten oder von Fachzentren durchgeführt. Eine Kombination aus
beiden wäre optimal. Es muss jedoch dafür Sorge getragen werden, dass kein
Abzweigen der Substanzen für den illegalen Konsum stattfindet, indem sich
Abhängige aus verschiedenen Quellen Verschreibungen beschaffen und dann
mit diesen Drogen handeln.
6. Der geschätzte Anteil der problematischen Opiatkonsumenten, die sich in der
EU in Substitutionstherapie befinden, schwankt zwischen einem Tiefstwert von
ungefähr 10 % und einem Höchstwert von über 50 % (siehe Tabelle 1, S. 3) [2].
Rua da Cruz de Santa Apolónia 23–25, P-1149-045 Lissabon • Tel. (351) 218 11 30 00 • Fax (351) 218 13 17 11 • http://www.emcdda.org
Überblick über die Substitutionstherapie
1. Ein wesentlicher
Bestandteil von
Drogentherapiesystemen
Es ist hinlänglich belegt, dass eine
Substitutionstherapie dazu beitragen
kann, die HIV-Übertragung, den
Drogenkonsum, das Risiko einer
Überdosis und die drogenbedingte
Kriminalität zu reduzieren sowie den
allgemeinen Gesundheitszustand der
Abhängigen zu verbessern. Eine
umfassende Literaturdurchsicht [3]
erbrachte das Ergebnis, dass die Rate von
HIV-Infektionen und Aids durch die
Methadontherapie dramatisch gesenkt
werden kann. Auch die Häufigkeit von
Heroininjektionen, die gemeinsame
Benutzung des Drogenbestecks und
die Arbeit in der Beschaffungsprostitution
können verringert werden. Eine deutsche
Vierjahresstudie [4] über eine ambulante
Methadontherapie hat gezeigt, dass der
Drogenkonsum abnahm, während sich
die sozialen Fertigkeiten und Beziehungen
verbesserten. Eine Evaluation der
Methadonsubstitution in Athen [5] zeigte
eine starke Abnahme des parallelen
Konsums von Heroin.
„In vielen Ländern hat sich die
Substitutionstherapie – nach
anfänglichem Widerstand – als
Maßnahme gegen das mit dem
intravenösen Konsum von Opiaten und
anderen Drogen verbundene Risiko einer
HIV-Infektion entwickelt. Ihr Nutzen ist
unter Beweis gestellt worden.
Neben anderen Maßnahmen zur
Schadensminimierung und einem
geschärften Bewusstsein hat sie Ende der
90er-Jahre in den meisten EU-Ländern
zur Eindämmung neuer HIV-Fälle unter
injizierenden Drogenkonsumenten
beigetragen.“
2. Substitution statt
Therapie?
Die Rechtsvorschriften zur
Substitutionstherapie in den meisten
EU-Ländern sehen vor, dass diese durch
psychosoziale Fürsorge unterstützt
werden sollte. Die Forschung zeigt, dass
die positiven Effekte der Therapie zum
Großteil auf solche Programme
zurückzuführen sind. Doch Theorie und
Praxis klaffen nur allzu oft auseinander –
der Schwerpunkt liegt häufig eher auf der
Substitution als auf der Therapie. Der
Bedarf an psychosozialer Fürsorge wird
durch Erkenntnisse aus der Forschung
belegt, denen zufolge Klienten in
Methadontherapie, wie andere
Drogenabhängige auch, einem
besonderen Risiko gegenüber psychischen
Erkrankungen und anderen
Gesundheitsproblemen sowie sozialer
Verelendung ausgesetzt sind [6].
Es sollte untersucht werden, inwieweit
die psychosoziale Fürsorge beim
Fortschreiten der Drogenkonsumenten
von Abhängigkeit zu Abstinenz
möglicherweise eine Katalysatorrolle spielt.
Die Versorgungsmöglichkeit von
Drogenkonsumenten mit psychischen
Gesundheitsproblemen hängt von den
Verbindungen zwischen psychiatrischen
Einrichtungen und Drogenfachstellen ab.
In einigen Ländern sind gute
Verbindungen mit spezialisierten
Dualdiagnose-Abteilungen hergestellt
worden. In anderen Ländern sind die
Verbindungen zwischen den betreffenden
Diensten weniger gut.
„Die Drogentherapie zielt darauf
ab, den Betroffenen zu
ermöglichen, die Kontrolle über
ihr Leben wiederzuerlangen.
Fachkräfte müssen fortlaufend
einschätzen, inwieweit die
Klienten, die
Ersatzverschreibungen erhalten,
bereit sind, durch einen
Entgiftungsprozess drogenfrei zu
werden. Die Bereitstellung
psychosozialer und praktischer
Hilfe während dieses Prozesses
ist besonders wichtig.“
3. Welche Ersatzsubstanzen
werden verwendet?
Nahezu alle EU-Mitgliedstaaten
verwenden eine vorherrschende
Ersatzsubstanz anstatt einer breiten
Palette von Substanzen [7]. Über 90 %
der Opiatsubstitution erfolgt in Form von
Methadon, außer in Frankreich, wo
überwiegend Buprenorphin verwendet
wird. EU-weit stieg die geschätzte Anzahl
von Drogenkonsumenten unter
Methadontherapie zwischen 1993 und
1997 um das Sechsfache an [1].
Die Ersatzsubstanzen haben
unterschiedliche Eigenschaften.
Buprenorphin birgt nicht die Gefahr einer
Überdosis; außerdem hemmt es die
Effekte eines parallelen Heroinkonsums.
Methadon hingegen ist einfach zu
verabreichen und kostengünstig – etwa 9
EUR pro Person pro Woche, im Vergleich
zu 65 EUR für Buprenorphin. Einige
Experten ziehen Buprenorphin für jüngere
Drogenkonsumenten und Methadon für
die langfristige Therapie älterer
Konsumenten vor. Buprenorphin scheint
auch besser für schwangere Frauen
geeignet zu sein und bei den
Neugeborenen weniger Probleme als
Methadon zu verursachen.
Herointherapieversuche laufen in
Deutschland und in den Niederlanden
und sind in anderen EU-Mitgliedstaaten
im Gespräch. Hierbei wird extrem
problematischen Heroinkonsumenten ihre
ursprüngliche Droge unter medizinisch
kontrollierten Bedingungen bereitgestellt.
Es ist bei allen Ersatzsubstanzen wichtig,
die Substitutionsdosis an die bisherige
Höhe des Drogenkonsums des Einzelnen
anzupassen.
4. Wie zugänglich ist die
Substitutionstherapie?
Trotz einer allgemeinen Ausweitung der
Substitutionstherapie in den letzten zehn
Jahren ist der Zugang zu ihr innerhalb der
EU weiterhin uneinheitlich. So scheint der
Erfassungsbereich in Griechenland,
Norwegen, Finnland und Schweden
begrenzt.
Die Substitution erfolgt fast ausschließlich
auf ambulanter Basis. Dies hat den
Vorteil, dass es kostengünstig ist und den
Drogenkonsumenten ermöglicht, ein
normales Alltagsleben zu führen.
Die Klienten, die sich in
Substitutionstherapie befinden, reichen
von relativ gut funktionierenden, häufig
berufstätigen Personen bis hin zu
marginalisierten und extrem
benachteiligten Drogenabhängigen auf
der Straße. Folglich benötigen manche
Klienten möglicherweise mehr Fürsorge,
als die ambulante Substitutionstherapie
leisten kann.
Die Zulassungskriterien unterscheiden sich
von einem EU-Land zum anderen
erheblich. Einige Programme und einige
Mitgliedstaaten – beispielsweise
Griechenland und Schweden – verfügen
über hochschwellige Dienste, die das
Alter, die Dauer der Drogenabhängigkeit,
die Anzahl der erfolglosen Therapien usw.
mit einbeziehen. Andere Mitgliedstaaten,
wie Dänemark, Spanien, Italien und die
Niederlande, schreiben als
Zugangskriterien lediglich
Opiatabhängigkeit und Therapiewunsch
vor. Durch den hochschwelligen Ansatz
werden Menschen mit ähnlichen
Problemen und Bedürfnissen erreicht;
dabei können allerdings diejenigen
ausgeschlossen werden, die zwar Hilfe
benötigen, den Zulassungskriterien jedoch
nicht entsprechen. Durch die
niedrigschwellige Methode werden die
meisten potenziellen Klienten erreicht,
wobei deren weit auseinander klaffende
Bedürfnisse jedoch nicht immer erfüllt
werden können. Idealerweise sollten
beide einander ergänzen. Auch bei der
Verfügbarkeit der Substitutionstherapie
in Haftanstalten gibt es sehr große
Unterschiede.
Land Geschätzte Prävalenz des Geschätzte Anzahl von Patienten
Belgien 20 200 7 000 (1996) 35 (3)
Dänemark 12 752-15 248 4 398 (4 298 Methadon, 100 Buprenorphin) 27-34
(1. Januar 1999) (4)
Deutschland 80 000-152 000 50 000 (2001) (4) 33-63
Griechenland keine Daten verfügbar 966 (1. Januar 2000) (4) –
Spanien 83 972-177 756 72 236 erhielten Methadon (1999) 41-86
Frankreich 142 000-176 000 71 260 (62 900 erhielten Buprenorphin
und 8 360 erhielten Methadon (Dezember 1999) (4) 40-50
Irland 4 694-14 804 5 032 (31. Dezember 2000) (4) 34-100 (5)
Italien 277 000-303 000 80 459 (1999) (4) 27-29
Luxemburg 1 900-2 220 864 [164 im offiziellen Programm und +/-700 38-45
Verschreibungen von Mephenon® (Methadon in
Pillenform) von praktischen Ärzten; 2000] (4)
Niederlande 25 000-29 000 11 676 (1997) 40-47
Österreich 15 984-18 731 4 232 (1. Januar 2000) (4) 23-26
Portugal 18 450-86 800 6 040 (1. Januar 2000) 7-33
Finnland 1 800-2 700 (6) 240 (170 Buprenorphin und 70 Methadon) 9-13
Schweden 1 700-3 350 (6) 621 (31. Mai 2000) (4) 19-37
Vereinigtes 88 900-341 423 (7) 19 630 6-22
Königreich
Norwegen 9 000-13 000 1 100 (2001) 8-12
(1) Methoden zur Einschätzung des problematischen Drogenkonsums schwanken erheblich zwischen den EU-Mitgliedstaaten. Weitere Einzelheiten zur nationalen
Prävalenz und zum problematischen Drogenkonsum siehe den Abschnitt über problematischen Drogenkonsum in Kapitel 1 (Jahresbericht der EBDD 2001) sowie
die Online-Tabelle 1 OL unter: http://annualreport.emcdda.org
Schätzungen des problematischen Drogenkonsums beziehen sich hauptsächlich auf Opiumkonsumenten, außer für Finnland und Schweden, wo der
Amphetaminkonsum kennzeichnend ist. In den vorliegenden Schätzungen für Finnland und Schweden sind keine Amphetaminkonsumenten enthalten.
(2) Geschätzter Anteil der problematischen Drogenkonsumenten in Substitutionstherapie.
(3) Die Prävalenzziffer umfasst nur injizierende Drogenkonsumenten, was zu einer Überschätzung der Substitutionserfassungsrate führen könnte.
(4) Unmittelbar vom nationalen Knotenpunkt gesammelte Information.
(5) Eine Substitutionserfassungsrate von 100 % scheint nicht plausibel, was darauf schließen lässt, dass die Prävalenzschätzung von 4 694 die derzeitige Prävalenz
unterschätzen könnte.
(6) Nur Opiatkonsumenten.
(7) Genauere Daten für das Vereinigte Königreich: Prävalenz des problematischen Drogenkonsums (Opiate) = 162 000-244 000; Klienten in der Substitutionstherapie =
35 000; Erfassungsrate = 14-22 %.
5. Wie wird die
Substitutionstherapie
durchgeführt?
Im Allgemeinen wird die
Substitutionstherapie entweder von
praktischen Ärzten durchgeführt oder von
Fachzentren, die über Dienste verfügen,
die speziell auf die Bedürfnisse der
Drogenabhängigen zugeschnitten sind.
Beides hat seine Vorteile: Die praktischen
Ärzte bieten einen breiten geografischen
Erfassungsbereich, während Fachzentren
über beträchtliche Erfahrung und
Fachwissen verfügen. In nahezu allen
EU-Mitgliedstaaten konzentriert sich die
Therapie jedoch auf die eine oder andere
Alternative. Eine Kombination aus beiden
– sowie gleichzeitig die Einrichtung
eines Systems, um die Abzweigung der
Substanzen für illegale Zwecke zu
verhindern – könnte wirksamer sein.
Beides hat auch seine Nachteile: Die von
praktischen Ärzten angebotenen
Dienstleistungen schwanken
beträchtlich, und die Drogenabhängigen
könnten sich unter Stammpatienten
unwohl fühlen. Fachzentren wiederum
sind geografisch nicht gleichmäßig
verteilt, was zu Nachteilen für
Drogenkonsumenten in entlegenen
Regionen führen könnte.
6. Drogenkonsumenten in
Substitutionstherapie
Tabelle 1 zeigt Schätzungen der Anzahl
von problematischen Drogenkonsumenten
(hauptsächlich Opiatkonsumenten) in der
EU und die geschätzten Prozentsätze in
Substitutionstherapie. Letztere schwanken
erheblich zwischen den Mitgliedstaaten.
In einigen Ländern liegen sie bei nur ca.
10 %, währen sie in anderen 50 %
überschreiten. Es ist zu beachten, dass es
bei den Schätzungen des problematischen
Drogenkonsums immer noch an
Genauigkeit fehlt und sie nicht leicht zu
vergleichen sind. Ein niedriger
Erfassungsbereich bedeutet, dass eine
große Anzahl von Drogenkonsumenten
möglicherweise einem erhöhten Risiko
einer Überdosis, von Gesundheitsschäden,
HIV und anderen Infektionskrankheiten
sowie der sozialen Ausgrenzung
unterliegt.
Man darf jedoch nicht vergessen, dass die
Substitution nur bei der Bekämpfung des
Problems des Opiatkonsums von Nutzen
ist. Für den Amphetamin- oder
Kokainkonsum gibt es keine derartige
Lösung. In den nördlichen EU-
Mitgliedstaaten entstehen größere
Probleme durch Amphetamine als durch
Heroin, und in der EU im Allgemeinen
lässt sich der Kokainkonsum nicht
ignorieren.
Trotz der Ausweitung der Substitutionstherapie
in den letzten Jahren berichten
die meisten Mitgliedstaaten nach wie vor
über einen Mangel an Qualitätskontrolle,
Überwachung und Evaluation einzelner
Programme.
Januar-Februar 2002
Schlussfolgerungen
Substitutionstherapie – politische Erwägungen
In der vorliegenden Kurzinformation zur Drogenpolitik werden einige der heute über den Stand der Substitutionstherapie in
der EU zur Verfügung stehenden Schlüsseldaten und Evaluationen zusammengefasst und die wichtigsten Quellen für
diejenigen angegeben, die mehr darüber wissen möchten. Ausgehend von den derzeitigen Erkenntnissen könnten folgende
Schlussfolgerungen die Grundlage für zukünftige politische Erwägungen bilden:
1. Die Substitution sollte als Teil eines umfassenden Therapiesystems für Opiatabhängige erachtet werden. In Ländern mit
einem hohen Übertragungspotenzial durch intravenösen Drogenkonsum sollte sie eine Schlüsselkomponente von
HIV-Präventionsstrategien darstellen.
2. Sie sollte systematisch durch psychosoziale Begleitprogramme unterstützt werden.
3. Das Angebot sollte eine breitere und diversifiziertere Palette von Substanzen und Dosierungen umfassen, um dem Profil
des sich in Therapie begebenden Klienten zu entsprechen.
4. Die Substitutionstherapie sollte verfügbarer und zugänglicher gemacht werden, wobei sowohl niedrigschwellige als auch
hochschwellige Optionen im Rahmen eines ausgeglichenen Ansatzes angeboten werden sollten.
5. Sowohl praktische Ärzte als auch Fachzentren sollten an der Durchführung beteiligt sein.
6. Der Anteil der in Substitutionstherapie befindlichen problematischen Drogenkonsumenten sollte regelmäßig in den
einzelnen geografischen Regionen überprüft werden, um die Durchführung der Dienstleistungen zu überwachen.
[1] Europäische Beobachtungsstelle für
Drogen und Drogensucht (EBDD)
(2000), Reviewing current practice in drugsubstitution
treatment in the European
Union, EMCDDA Insights Nr. 3,
Amt für amtliche Veröffentlichungen der
Europäischen Gemeinschaften,
Luxemburg 2000.
(Enthält eine umfassende Bibliografie zum
Thema Substitutionstherapie.)
[2] Europäische Beobachtungsstelle für
Drogen und Drogensucht (EBDD)
(2001), Jahresbericht über den Stand der
Drogenproblematik in der Europäischen
Union 2001, Tabelle 1:
Substitutionsbehandlung bei
problematischen Drogenkonsumenten,
Amt für amtliche Veröffentlichungen der
Europäischen Gemeinschaften,
Luxemburg 2001, S. 33.
[3] Drucker, E., Lurie, P., Wodak, A.,
und Alcabes, P. (1998), „Measuring harm
reduction: the effects of needle and
syringe exchange programs and
methadone maintenance on the ecology
of HIV“. Aids, 12 (suppl. A),
S. 217-230.
[4] Küfner, H., Vogt, M., und Weiler, D.
(1999), Medizinische Rehabilitation und
Methadon-Substitution, Schneider Verlag
Hohengehren, Baltmannsweiler.
[5] EDDRA-Datenbankeintrag (2001),
Second unit of the methadone
substitution programme in Athens,
(http://www.reitox.emcdda.org:8008/
eddra), EBDD, Lissabon.
[6] Farrell, M., Howes, S., Taylor, C.,
Lewis, G., Jenkins, R., Bebbington, P.,
Jarvis, M., Brugha, T., Gill, B., und
Meltzer, H. (1998), „Substance misuse
and psychiatric co-morbidity: an overview
of the OPCS national psychiatric morbidity
survey“. Addictive Behaviors, 23, Nr. 6,
Elsevier Science Ltd., Oxford, S. 909-918.
[7] Europäische Beobachtungsstelle für
Drogen und Drogensucht (EBDD)
(2000), Jahresbericht über den Stand der
Drogenproblematik in der Europäischen
Union 2000, Tabelle 1: In der EU
verwendete Ersatzsubstanzen,
Amt für amtliche Veröffentlichungen der
Europäischen Gemeinschaften, Luxemburg,
2000, S. 37.
OFFIZIELLER HERAUSGEBER: Amt für amtliche Veröffentlichungen der Europäischen Gemeinschaften
© Europäische Beobachtungsstelle für Drogen und Drogensucht, 2002
DIREKTOR: Georges Estievenart
REDAKTION: Kathy Robertson, John Wright
AUTOREN: Margareta Nilson, Ulrik Solberg, Danilo Ballotta, Lucas Wiessing
GESTALTUNG: Dutton Merrifield, UK
EUR
Printed in Italy
Informationen im WWW
Ich habe das auch als File fuer die Tabellen: att_33470_DE_Dif01de
BINGHAM, Me. — The orange signs posted throughout Chet Hibbard’s pharmacy here relay a blunt warning: We Do Not Stock OxyContin.
“Outside hiring an armed guard to be in here 24/7, I don’t know what else to do.” CHET HIBBARD, a Maine pharmacist who has stopped selling OxyContin.
Mr. Hibbard stopped dispensing the highly addictive painkiller last July, after two robbers in ski goggles demanded it at knifepoint one afternoon as shocked customers looked on. It was one in a rash of armed robberies at Maine drugstores last year, a sharp increase that has rattled pharmacists and put the police on high alert.
“I want people to know before they even get in the door that we don’t have it,” Mr. Hibbard said of OxyContin, which the authorities say is the most common target of pharmacy robberies here. “Outside hiring an armed guard to be in here 24/7, I don’t know what else to do.”
Maine’s problem is especially stark, but it is hardly the only state dealing with pharmacy robberies, one of the more jarring effects of the prescription drug abuse epidemic that has left drugstores borrowing heist-prevention tactics from the more traditional targets, banks. In at least one case, a tiny tracking device affixed to a bottle let the police easily track a thief after a robbery.
More than 1,800 pharmacy robberies have taken place nationally over the last three years, typically conducted by young men seeking opioid painkillers and other drugs to sell or feed their own addictions. The most common targets are oxycodone (the main ingredient in OxyContin), hydrocodone (the main ingredient in Vicodin) and Xanax.
The robbers are brazen and desperate. In Rockland, Me., one wielded a machete as he leapt over a pharmacy counter to snatch the painkiller oxycodone, gulping some before he fled. In Satellite Beach, Fla., a robber threatened a pharmacist with a cordless drill last week, and in North Highlands, Calif., a holdup last summer led to a shootout that left a pharmacy worker dead.
The crime wave has spurred pharmacists to tighten security measures and add ones they may never have imagined. Many have upgraded their surveillance cameras; some have installed bulletproof glass and counters high enough to keep would-be robbers from jumping them, giving these pharmacies the aesthetic of an urban liquor store. In Tulsa, Okla., where there was a steep increase in drugstore robberies last year, at least one pharmacist now requires customers to be buzzed in the door.
Meanwhile, the police are quietly experimenting with new tools. In Lewiston, Me., last fall, a Rite Aid pharmacist handed a robber who threatened to shoot her five bottles of OxyContin, including one that contained a tracking device.
According to court records, the device led the police to the suspect’s home on a rural road shortly after he fled the store. They gathered evidence there, arrested the suspect a few days later and indicted him last month.
The Drug Enforcement Administration does not routinely investigate reports of pharmacy robberies, and therefore “it cannot be determined what factors are contributing to these types of thefts,” a spokeswoman said.
But some local law enforcement officials have been overwhelmed enough by the incidents to seek help. Thomas Delahanty II, the United States attorney in Maine, announced recently that the federal authorities would help investigate the heists from now on and prosecute some of the cases.
Federal charges could bring more prison time, Mr. Delahanty said, describing the surge in such robberies as “staggering numbers that can’t be ignored.” There were 21 in Maine last year, according to the D.E.A., up from two in 2008 and seven in 2009.
In Biddeford, Me., a city of 21,000 that has had seven pharmacy robberies since December 2009, Roger Beaupre, the police chief, said he was urging the stores to require customers to remove hoods and sunglasses before entering and to consider caging in their pharmacy counters.
Police officers there got free training in how to investigate pharmacy heists last month from Purdue Pharma, the maker of OxyContin. The company also trains pharmacists on how to prevent robberies and what to do should they fall victim to one, said Rick Zenuch, its director of law enforcement liaison and education.
“The very first tip we give them is comply, comply, comply,” Mr. Zenuch said. “Do exactly what the suspect wants, to end the encounter as soon as possible.”
In Washington State, where more than 100 pharmacy robberies have taken place over the last three years, law enforcement officials say the penalty for second-degree robbery, when the pharmacist may be threatened but no weapon is shown, is too weak. Dan Satterberg, the King County prosecutor, said he had submitted a bill to the Legislature to increase the minimum jail time to three years from three months.
“Word travels fast on the street about what an easy target the pharmacies are and how much profit can be made and what small punishment is attached,” Mr. Satterberg said.
OxyContin goes for $1 a milligram on the street, Mr. Satterberg and other law enforcement officials said, and the most popular pill is 80 milligrams.
Many pharmacies in Washington have deterred would-be robbers by putting time-release locks on the safes where they store narcotics and staggering their inventory, Mr. Satterberg said. Perhaps as a result, the number of armed robberies at pharmacies there dropped to 23 in 2010 from 49 in 2008, according to the D.E.A.
Still, Mr. Satterberg said, the threat of robbery has made it difficult for retail chains in the state to recruit enough pharmacists in recent years.
“They feel very vulnerable when so many people are so desperate to get what they keep behind those counters,” he said.
In sheer numbers, Florida, Indiana, California, Ohio and Washington have had the most armed robberies of pharmacies since January 2008, according to the D.E.A. But Maine, Oklahoma and Oregon had the sharpest increases last year.
All but a handful of the Maine robberies took place at Rite Aid and CVS stores, some of which were hit multiple times.
In Tulsa, Okla., where pharmacy robberies last year far outpaced bank robberies, the police said the crimes were now more often committed by gangs who want to sell the drugs than addicts in search of a fix. Robbers there often demand Xanax, an anti-anxiety drug, along with opioids, said Sgt. Dave Walker, who runs the robbery unit of the Tulsa Police Department.
In Bingham, a remote town of about 1,000, the men who robbed Mr. Hibbard’s pharmacy, E.W. Moore & Son, were caught and sent to prison, as was another robber who held up the store at gunpoint in 2006. But despite that comforting fact and the store’s nine surveillance cameras and high-tech alarm system, Mr. Hibbard and his employees still jump when the place is quiet and they hear footsteps coming up the ramp, they said.
“I stood right between him and his knife,” said Lori Pratt, a pharmacy technician, referring to one of the robbers. “I was all ready to go on the Internet after it happened and get a Taser gun.”
Unlike Mr. Hibbard, Rite Aid has chosen to keep stocking the drugs that are popular with robbers, said Eric Harkreader, a spokesman. But the company now limits the amount of certain drugs in stores at any given time.
“If they are going for lots of quantity at once, we don’t want to help them out,” he said. “But we certainly want to have the prescription available for all its legitimate purposes.”
In Biddeford, a Rite Aid that was robbed twice last year was struck again last week. The suspect, who demanded OxyContin and fled into the night, remains at large.
source: http://www.nytimes.com/2011/02/07/us/07pharmacies.html?_r=1&pagewanted=2
20% of US adults get prescriptions for analgesics, yet little is known about the safety of these drugs. In recent years, a number of high profile lawsuits have caused an upheaval in the public’s trust of prescribed pain medication. If you haven’t been concerned about the safety of your pain medications, you should be.
According to Solomon, et. al, authors of „The Comparative Safety of Analgesics in Older Adults With Arthritis“, published in Archive of Internal Medicine this month, most randomized clinical trials – which includes studies the FDA requires of a drug maker before their product can be sold on the market – look at how well a pain med works, but NOT how safe it is. They say that most of the time, study subjects are healthy, unlike the people for whom the drug is meant. Add to this the fact that as a general rule, long term side effects are rarely evaluated in studies, and you have cause for doubt about pain med safety, in my opinion.
Two studies evaluating health risks associated with taking pain meds made the news recently. The news reports I read focused on the findings that giving opioids (narcotic pain medications) to people over the age of 80 increased their risk of complications, health problems and even death. Of course, conventional pain doctors who commented in the news reports tried to refute the results by saying the study had serious problems with confounding. Little information about exactly what skewed the results was given in the news reports.
Confounding happens when a researcher observes people to find out what causes or at least is associated with a particular effect. Investigators may hypothesize that one characteristic is responsible for a disease or condition. But another characteristic, related to the one they are evaluating, emerges as a possible cause during the course of the study. So the hypothesis just got more complicated. In the two recent studies, confounders included any possible role that obesity, smoking, drinking and the use of over the counter pain meds (NSAIDs) may have played in the safety of those who took opioids or Cox-2 inhibitors. In other words, the researchers were unable to factor these things in when they looked at safety events resulting in hospitalization and/or death in seniors taking opioid pain medication.
The study authors talked about this problem in their report, acknowledging the possibility that something other than the medication was at work here. They described the way in which they created comparable groups of pain med taking seniors. And as it turns out, these remaining factors (smoking, drinking, being overweight and taking NSAIDs) occupied only a small fraction of the overall possible causes of the health risks identified in the two studies.
The study compared opioid use to NSAID use, as well as to the use of Cox-2 inhibitors.
The studies found that:
Hopefully these studies will trigger more safety studies, but the authors rather doubt that.
As with most studies, the authors end by saying more studies are necessary before we can definitely know the best course of action for patients.
Sources:
Solomon, D. MD, et. al. The Comparative Safety of Analgesics in Older Adults With Arthritis. Arch Intern Med. Vol 170 Dec 13/27 2010. Accessed: Dec 21 2010.
I recently saw a copy of Amar Farooqui’s book, Opium City. It revealed a historical detail that is very difficult to swallow: Mumbai’s prosperity is rooted in the Opium Trade of the 19th century. Some of the most respected business families today owe their fortune to that vile practice. Some of the city’s memorable buildings were financed by this terrible trade.
Illustration/ Devdutt Pattanaik
So what was this Opium Trade? The British East Indian company was one of the first companies in the world that had ’shareholders‘. To pay shareholders, the company had to make huge profits. So the Company forced Indian peasants to grow opium, instead of grain. This opium was sold in China in exchange for highly profitable tea. So India became poor, an entire generation of Chinese became opium addicts, to make the Company, and later the Empire, rich.
The best quality opium was grown in Malwa and since much of India then was not quite under the Company’s control, the only way to access this opium was to smuggle it via Rajasthan and Karachi to the Bombay fort.
Many now respectable Indian business families (allegedly and apparently, for everyone denies it now) participated in this lucrative trade and made huge fortunes.
When I watch films like Young Victoria, King’s Speech and The Queen I can’t help but feel this is subtle propaganda to re-establish the nobility of a tethering British royal family, and I wonder if the rulers portrayed ever took responsibility for the Opium Wars that filled their coffers as they blessed and taxed and finally controlled the East India Company’s shareholders. Likewise, do we?
I imagine Chinese students being taught this history: How the West abused it for its profit and how Indian business families participated in their downfall. This could be the reason why the Chinese do not have a great relationship with India, and look at everyone with suspicion. How does one rectify it?
They say children inherit the sins of the father. The Mahabharata refers to this concept again and again. How crimes committed in an earlier generation end up affecting a later generation. The epic begins with the story of Janamejaya angry that his father has been killed by a snake, until he is told that his great grand parents destroyed an entire forest that was home to thousands of snakes. Even the horrific war at Kurukshetra, like the World Wars, is not merely the fight of cousins, but the outburst of several generations of rage and denial and frustration and envy. That is why these stories look not at one generation but at several.
So long is the history and so deep is the wound that everyone assumes they are the victims and no one is prepared to take the responsibility of the villain. Such is life. There are no heroes or villains, just people who choose to exploit, people who seek retribution, people who cannot forgive and people who yearn shy away from responsibility but yearn for nobility.
he growing of opium poppies in the Afghan provinces of Helmand and Kandahar is predicted to be down for the second year running.
But a UN drugs forecast released on Monday says that poppy growing will increase elsewhere in Afghanistan.
Forecasting the Afghan crop is a tricky business, and the groundwork for this UN survey is based on the sample of only a few villages in each province.
But matched with satellite imaging, it suggests poppy growing will spread.
And that spread this year will even extend into provinces that had become poppy-free in recent years.
The United Nations Office on Drugs and Crime (UNODC) has expressed concern in particular about a predicted increase in Nangahar, a large province bordering Pakistan where poppy growing had been all but eradicated in recent years.
It is a strange market that does not conform to usual market forces.
Although the price to farmers more than doubled last year to $164 a kilogram – because of a cut in output caused by crop disease – the price paid by buyers abroad did not go up.
When you see more conflict, when you see more poverty, you will see more opium cultivation” End Quote Jean Luc Lemahieu UNODC head in Kabul
So Afghanistan’s drug barons were squeezed in the middle.
The higher prices paid to farmers played a big part in encouraging more to plant this year.
The UN survey predicts more planting across a wide swathe of central Afghanistan – from Herat and Ghor in the west to the provinces east of Kabul along the Pakistan border.
Their forecast for the northern region will come out later in the year, as the season starts later in the north.
The predicted rise in poppy planting tallies with other evidence suggesting that the Taliban insurgency has spread across a wider region of the country.
The UNODC’s head in Kabul, Jean Luc Lemahieu, said tough measures were needed so that the forecast did not become a reality.
„When you see more conflict, when you see more poverty, you will see more opium cultivation. That is why we continue saying this is not business as usual. We need to put extraordinary measures in place today,“ he said.
The silver lining in the forecast is that for the third year running, Helmand’s crop is forecast to reduce this year – and for the second year, Kandahar too will grow fewer poppies.
Foreign troops
These two provinces are by far the largest poppy-growing regions in Afghanistan – accounting for more than a third of the world’s opium between them.
The surge of US troops along with British troops in the main population centres in Helmand played a big part, as did weather conditions – too cold and dry at the time farmers wanted to plant.
But the deputy head of the British mission in Helmand, Leo Tomlin, said the forecast showed that a set of policies were working.
They include public information, strong leadership from the Governor Gulab Mangal, tougher policing and better job opportunities.
„It’s almost an aligning of the stars. That’s also why counter-narcotics takes a long time. It’s not something you can start one year and expect to see immediate results,“ he said.
„It’s something that needs a long-term investment, a continued investment with a very similar type of predictable programme.“
Even these predicted reductions will leave more than 65,000 hectares under cultivation for poppies in Helmand and some 25,000 hectares in Kandahar.
It may have been pushed onto marginal land, out of sight, but it still remains a potent threat to stability and security in Afghanistan.
Jan 31, 2011, 14:14 GMT
Kabul – The United Nations said Monday in a report that the increasing price of opium had not boosted its cultivation in the main producing provinces of southern Afghanistan.
It also said opium growing was ’strongly associated with insecurity and lack of agricultural assistance.‘
The current high price of opium did not produce an increase in opium cultivation in the biggest producing provinces of Helmand and Kandahar, the report titled Afghanistan: Opium Survey 2011 said.
The opium winter assessment report prepared by the United Nations Office on Drugs and Crime and the Afghan Counter Narcotics Ministry also predicted a decrease in the opium cultivation in the two southern provinces in 2011.
The UN report said the reasons for decreasing cultivation could be dry climate conditions leading to crop failure, a changing political environment, increasing government control and more military operations by Afghan and international troops around the time of poppy planting which ‚may have‘ discouraged the farmers.
NATO-led forces with Afghan security personnel have been pushing the Taliban from the areas around Kandahar and Helmand since 2010 with ’some gains‘ in the region.
In other parts of Afghanistan, mainly the western, eastern and central provinces, the report observed an increase.
The UN report warned of ‚increasing cultivation trends‘ in the western and eastern regions, especially in Nangarhar, bordering the highly volatile Khyber-Pakhtunkhwa area in Pakistan, and said it has ‚the potential to be a major poppy cultivating province.‘
The report studied the first phase of the assessment for December and January.
‚Villages with a low level of security and which had not received agricultural assistance in the previous year were significantly more likely to grow poppy in 2011 than villages with good security and those which had received assistance,‘ the report said.
Earlier this month, the UN drug agency had said that rising opium prices could drive up Afghanistan’s production area in 2011 for the first time in four years.
The price went up by 164 per cent in 2010. The total harvest was nearly halved due to bad weather conditions and a plant disease.
Afghanistan is the world’s biggest opium-producing country with a global share of 77 per cent. At least 1.7 million farmers are directly engaged in the cultivation of poppy farms, according to the UN.
For the Taliban insurgents, poppy production is one of the main sources of income which funds their insurgency.
Poppy field in Afghanistan
31 January 2011 – Poppy cultivation in Afghanistan is expected to decline slightly this year despite the current high prices of opium, the United Nations Office on Drugs and Crime (UNODC) said today, basing the information on a qualitative assessment of farmers’ intentions in the Asian country.“The findings of the Opium Winter Rapid Assessment Survey in the southern region are encouraging,” said Yury Fedotov, the Executive Director of UNODC.
“A combination of factors seemed to have contributed to this development – dry weather, efforts directed against poppy cultivation and towards increasing government control, as well as licit alternatives to poppy,” he added.
Planted poppy seeds start to germinate in winter in the main opium producing provinces in the southern, western and eastern areas of Afghanistan, while sowing takes place later in the north, according to UNODC.
The expected decline in opium cultivation, as well as prolonged drought in the south may lead to another year of reduced opium production, the agency said. An outbreak of opium blight last year cut production by half and caused prices to soar.
The survey once again highlighted the direct correlation between insecurity, lack of agricultural aid and opium cultivation, UNODC noted. Villages considered insecure and lacking agricultural assistance are more likely to grow poppy this year than those with better security and assistance.
An estimated 90 per cent of insecure villages are involved in opium cultivation, while those targeted by anti-poppy awareness campaigns are significantly less likely to grow poppy, the agency reported.
Los Angeles – Subkutane Implantate könnten die Compliance der Opiatabhängigen bei der Buprenorphin-Substitution verbessern und einen Schwarzmarkt verhindern. Eine Phase-III-Studie im US-amerikanischen Ärzteblatt JAMA 2010; 304: 1576-1583) attestiert dem Präparat eines US-Herstellers jetzt eine passable Wirksamkeit.
In der Substitutionstherapie von Heroinabhängigen ist Buprenorphin eine attraktive Alternative zu Methadon. Denn der partielle Opiat-Agonist ist weniger anfällig gegenüber Überdosierungen und auch außerhalb der großen Substitutionszentren verfügbar. In vielen Ländern ist die sublinguale Buprenorphin-Substitution deshalb sehr beliebt.
Es lässt sich allerdings kaum verhindern, dass das starke Opiat auf den Schwarzmarkt gelangt – selbst wenn es in vielen Ländern mit dem Antagonisten Naloxon versetzt ist. Bei einer unzuverlässigen Einnahme kommt es außerdem schnell zu Entzugssymptomen und die Rückfallquote der Patienten ist deshalb hoch.
Beide Probleme könnten durch subkutane Implantate gelöst werden, die den Wirkstoff über mehrere Monate kontrolliert freisetzen. Das Präparat eines US-Herstellers wurde jetzt an 18 Behandlungszentren des Landes in einer Phase-III-Studie untersucht.
108 Patienten – zu zwei Drittel Heroin-, zu einem Drittel Medikamentenabhängige – wurden jeweils vier 26 mm lange und 2,5 mm dicke Implantate in 2 bis 3 mm Tiefe ins Unterhautfettgewebe am Arm eingebracht.
Wenn notwendig konnten die Probanden ein fünftes Implantat erhalten. Nach 6 Monaten wurden alle Implantate entfernt, was einen kleinen chirurgischen Eingriff erfordert, der eine kurze Narbe hinterlässt. In einer Vergleichsgruppe von 55 Patienten wurden Implantate mit Placebo implantiert, was ethisch gerechtfertigt war, weil die Patienten in beiden Gruppen bei Bedarf zusätzlich Sublingualtabletten mit Buprenorphin erhalten konnten.
Wie Walter Ling von der Universität Los Angeles und Mitarbeiter berichten, erhöhten die Buprenorphin-Implantate den Anteil der negativen Urinkontrollen – als Hinweis auf einen fortgesetzten Drogenkonsum – von durchschnittlich 28,3 auf 40,4 Prozent.
Auch in den sekundären Endpunkten wurde eine Wirksamkeit nachgewiesen: Insgesamt 65,7 gegenüber 30,9 Prozent nahmen bis zum Schluss an der Studie teil. Auch die Häufigkeit von Entzugssymptomen wurde ebenfalls signifikant gesenkt.
Im Buprenorphin-Arm gab es keine Therapieversager: Alle kamen mit vier oder fünf Implantaten aus. Im Placebo-Arm wurden 30,9 Prozent der Patienten als Therapieversager eingestuft, weil sie häufiger als dreimal in der Woche Sublingualtabletten nachfragten.
Die Implantate lösten nur geringe Lokalreaktionen aus, wobei es zwischen Buprenorphin und Placebo keine Unterschiede gab. Der Hersteller führt derzeit eine zweite Phase-3-Studie durch und will sich nach deren Abschluss um eine Zulassung in den USA und in Europa bemühen. © rme/aerzteblatt.de
ScienceDaily (Feb. 1, 2011) — Opiate abuse is a chronic disorder and maintaining abstinence represents a major challenge for addicts.
Individuals recovering from opiate dependence have long reported that while the acute withdrawal symptoms from opiates may pass relatively quickly, they do not feel quite right for several weeks or even months thereafter. Called the „protracted abstinence syndrome,“ this cluster of vague depressive-like symptoms can include reduced concentration, low energy level, poor sleep quality, and anhedonia.
New data in animals, reported in Biological Psychiatry, now implicates the serotonin system in this phenomenon.
French researchers found that mice with chronic morphine exposure showed decreasing physical dependence during a period of abstinence, with no physical withdrawal symptoms after 4 weeks. In contrast, low sociability and despair behavior clearly developed after 4 weeks of abstinence.
Remarkably, treatment during the abstinence period with the antidepressant fluoxetine prevented the development of both social aversion and despair behavior.
This is important because fluoxetine targets the serotonin system, which is known to influence mood.
Senior author Dr. Brigitte Kieffer explained that this study „establishes a direct link between morphine abstinence and depressive-like symptoms, and strongly suggests a causal effect of serotonin dysfunction in depressive features associated with abstinence.“
„The greatest risk associated with protracted abstinence is relapse to drug use,“ comments Dr. John Krystal, Editor of Biological Psychiatry. „This study provides new insights into a process that may contribute to relapse.“
These findings should foster novel research along serotonergic pathways in drug abuse. It is hoped that these findings can lead to real-world clinic use, since serotonergic medication is already broadly available.
source; http://www.sciencedaily.com/releases/2011/02/110201083930.htm
Abstract: Self-injurious behavior (SIB) is a primary reason that individuals with
neurodevelopmental disabilities (NDD) are either retained in restrictive environments or
are administered psychotropic medication. There are no known causes and no universally
accepted treatments for this complex behavior among individuals with NDD. There is
developing evidence, however, that individuals exhibiting SIB have a disturbance of the
opiate-mediated pain and pleasure system. One hypothesis is that SIB reflects insensitivity
to pain and general sensory depression (hypoalgesia), perhaps related to chronic elevation
of endogenous opiates. For instance, many self-injurious individuals do not exhibit the
usual signs of pain after their “injurious” behavior. Moreover, for some individuals the
addictive properties of elevated endogenous opiates (euphoria) may be responsible for
maintaining their SIB. In this perspective, SIB may be viewed as an addiction because it
supplies the „fix“ for tolerant, down-regulated opiate receptors. Reports that levels of
endogenous opiates at rest and after SIB episodes predict positive responses to opiate
blockers (e.g., naltrexone) provide further support for opiate-mediated SIB and form the
basis for a rational treatment strategy. Although the long term effects of opiate blockers on
SIB are unknown, reduction in SIB following acute treatment provides support that a specific
biological system may be dysregulated in a subgroup of patients. It is concluded that
naltrexone produces a clinically significant reduction in the serious and life-threatening
behavior of self injury for individuals who have not been responsive to any other type of
treatment. Several suggestions and cautions are provided for regimens of naltrexone
treatment of SIB.
1. Introduction
Despite considerable research effort, self-injurious behavior (SIB) continues to be a primary reason,
together with aggression toward others, that individuals are either retained in institutional (restrictive)
environments or are administered psychotropic medication. Today, SIB remains unmanageable,
expensive ($150,000–$500,000/year/patient in institutional settings, with national costs well over
$3,000,000,000 [1]), and is often life threatening. It is surprisingly prevalent, occurring in ~30% of
individuals with developmental neurological complications, including those with autistic disorders [2,3].
Twenty-five experts invited by the National Institute of Child Health and Human Development
(NICHD) to discuss the relations among the genetic, neurobiological, and behavioral causes and
treatments for SIB reached two general conclusions. Intentional acts of harm to self, evident in many
species, (a) have no known cause and (b) no agreed upon treatment [4]. The apparent absence of
visible progress in understanding or treating SIB is not because of a lack of interest or effort. Studies of
self-injury have increased exponentially over the past 30 years, rising from just 60 published studies
between 1980 and 1984 to over 1,700 studies reported between 2005 and 2010 (Figure 1).
Figure 1. Number of studies of self-injurious behavior (SIB) conducted in 5-year intervals
from 1980 to the present.
One major obstacle in understanding the mechanisms of SIB and developing coherent treatment
plans is the absence of distinctive behavioral phenotypes. Despite the consensus that SIB has variable
expression with no known cause, the group of NICHD experts agreed that SIB could be defined,
perhaps with greater precision than most complex human behaviors. SIB is a directly observable
behavior that can be reliably counted. The NICHD group argued that data collection and analysis had
advanced so that complex patterns of SIB should replace or supplement measures of rate and
frequency [5,6]. Two distinct patterns of SIB were proposed as possible guides. One pattern consists of
bouts that are most likely maintained by environmental contingencies. The second pattern involves
protracted periods of SIB that are most likely under the primary influence of biological factors. The
vast majority of existing studies, however, have reported frequencies or rates of occurrence of SIB
often linked to a single environmental manipulation. It is a significant advantage that many forms of
SIB can be counted and time-stamped enabling contemporary studies to use sequential and time series
procedures to define their structure and their relations with other behaviors and the environment. We
subjected extensive and lengthy observations of maladaptive behavior in its natural environmental
context to time series analysis and discovered unique temporal and sequential patterns of these severe
maladaptive behaviors [2,3,7-10].
Specifically, we found for a large majority of the individuals studied, SIB was predicted only by its
own recent history. In our cohort of severely self-injurious patients, SIB was expressed consistently in
successive occurrences revealing a unique pattern of sequential dependence compatible with a
“contagious” distribution. Application of time-series methods of analysis that controlled for chance
pairings of events indicated that the contagious patterns of SIB were independent from frequency and
rate of occurrence. That is, the temporally dependent patterns we observed were not a function of high
rates of occurrence. Moreover, and surprisingly, SIB was not associated consistently with other
behaviors or with the several staff activities or environmental conditions recorded in these studies.
Thus, in a significant majority of these individuals, SIB episodes were self-perpetuating and not related
to antecedent or subsequent environmental circumstances, events, or other recorded behaviors.
This novel and surprising finding was consistent with conclusions of the NICHD group that some
expressions of SIB may have an underlying biological basis because a solely self-perpetuating
behavior is most parsimoniously explained by internal (i.e., biological) motives [2,11-13]. The vast
majority of individuals in our cohort exhibited the most primitive level of internally regulated behavioral
patterns despite years of behavioral interventions and treatment with various medications [8,9].
Anecdotal and clinical observations of these individuals also strongly suggested a biological basis for
their behavior and specifically involvement of the pain and pleasure systems. Typically, SIB is
repetitious consisting of hourly, daily, weekly, monthly, or even yearly cycles [14]. Some individuals
who repeatedly injure themselves appear immune to the normal experience of pain [12]. They abuse
and injure their bodies, hitting or biting themselves, hurling themselves to the ground, and banging
their head against solid objects resulting in broken bones, disfigurement, blindness, and even loss of
life [2,15,16]. They often work to overcome interventions designed to decrease self-injury in a manner
that is consistent with seeking positive reward. For instance, protective devices (such as helmets) may
result in individuals exerting greater effort and exhibiting greater rates of behavior to hit and harm
themselves [17].
Because many medications that treat pain or induce pleasure are addicting, it is interesting that SIB,
in addition to the obvious involvement of pain systems, shares features of addiction such as
compulsive and ritualistic (or stereotypic) patterns that either comprise or surround the self-injuring
acts. One biological system that has been implicated in SIB and the modulation of pain and pleasure is
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the hypothalamic-pituitary-adrenal (HPA) stress axis and specifically the proopiomelanocortin (POMC)
molecule [3,18,19].
2. The Biological Stress System Pain, Pleasure, and SIB
Thompson and Caruso [6] recognized that some forms of SIB were “neurochemically driven and
independent of environmental events.” Early studies either of basal or of resting levels of a variety of
peptides, proteins, transmitters, and amines in plasma or cerebrospinal fluid from patients exhibiting
SIB, however, generated inconclusive results. This was not surprising because there was little
consistency among studies regarding the rigor of diagnosis, the molecule measured, the tissue assayed,
or the conditions assessed [20-26].
2.1. Pain and the Endogenous Opioid System
Although it is not a universal observation, most self-injurious individuals do not exhibit the usual
signs of pain after their “injurious” behavior. Despite inflicting serious physical damage to their bodies,
many of these individuals do not grimace, cry, or show other symptoms that they are experiencing pain.
It has been suggested that this absence of response to self-inflicted injury reflects insensitivity to pain
and general sensory depression induced either by elevated endogenous opiates or by supersensitive
opiate receptors [11,27-29]. This possibility is supported by classical findings that opiate receptor
blockers (a) reverse congenital insensitivity to pain [30]; (b) normalize hypothalamic-peptide
dysfunction coexisting with elevated pain threshold [31]; and (c) increase brain responses to sensory
information [32]. These observations are consistent with a venerable animal literature proving that
opiate blockers lower pain threshold [33]. In summary, these findings support an analgesia (or pain)
hypothesis that implies that self-injurious individuals do not feel pain because of chronically elevated
endogenous opiates and/or opiate receptor downregulation.
2.2. Pleasure (Addiction) and the Endogenous Opioid System
It also is possible that the addictive properties of elevated endogenous opiates are responsible for
maintaining SIB. If it is presumed SIB does result in pain and that the experience of pain results in the
release of opiates, then it can be argued that individuals commit self-inflicted harm to receive the
euphoric (pleasurable) effects of increased circulating opiates. From this perspective, SIB is an
“addiction” to the endogenous opiate system because its consequences supply a “fix.” It has been
known for over 25 years that endogenous opiates have addictive properties as indicated by the
development of tolerance [34], physical dependence [35], and euphoric-like effects [36] after repeated
administration. The repetitive, often compulsive, and ritualistic patterns of SIB (i.e., injury to one area
of head or body, stereotyped patterns of behavior, and catastrophic responses if the environment is
slightly changed) are similar to rituals and compulsive patterns often associated with addictive
behaviors. The addiction hypothesis maintains that individuals with SIB may endure the pain to enjoy
the pleasure it produces as well as to avoid a withdrawal effect. The addiction hypothesis predicts that
SIB may be reinforced both positively and negatively because it gains the individual access to the
narcotic effect of endorphins while simultaneously allowing the individual to escape the unpleasant
sensory consequences commonly associated with the absence of opiates following chronic and
sustained access.
2.3. Stress and the Endogenous Opioid System
The endogenous opioid system is tightly coupled with the general stress response. Evidence from
several laboratories indicates that functioning and processing of a stress-related molecule (POMC) in
the HPA axis may be perturbed among subgroups of individuals exhibiting SIB [15,19,21,37-43]. In
humans, most POMC is produced in the pars distalis of the anterior pituitary but also by hypothalamic
neurons and neurons in the amygdala and pituitary stalk. POMC is a well-characterized 31-K dalton,
bioinactive protein-like molecule that is post-translationally converted by enzymes (e.g., PC1 and PC2)
into biologically active fragments, including B-endorphin (BE) and adrenocorticotropic hormone (ACTH)
[15,44-48]. Normally, BE is coreleased from the anterior pituitary with ACTH in response to a variety of
stressors. However, elevated BE but not ACTH is associated with SIB either at rest or after an episode of
SIB [3,12,18]. This suggests that one consequence of SIB is the disregulation of the arousal system. The
validity of these hypotheses is not known but they have encouraged treat-ments, including opiate
receptor blockers, designed to regulate the opiate/stress system as means to control SIB.
3. Efficacy of Opiate Blockers in the Treatment of SIB
3.1. Acute Effects of Naltrexone
In a review of pre-1991 studies [49], six of eight published studies reported that injectable naloxone
significantly reduced SIB. In these eight studies, naloxone was tested in a total of ten individuals with
SIB. A decrease in SIB was reported for seven individuals. In that same review, 12 published studies
of naltrexone (Naltrexone) in MR/DD individuals were summarized. Most of the studies either were
case studies or were studies with very small samples. At that time, 45 MR/DD individuals (at least 28
with SIB) had been treated with naltrexone and 38 individuals had positive responses of various
degrees including a reduction in SIB in 24 of the 28 patients. A separate review of 13 studies
(including several in the Sandman review [49]) concluded that about one-third of the patients tested
with Naltrexone had a decrease in their SIB [50]. Several studies in this later review included juvenile
patients under the age of 8 years [51] and patients with primary behavioral problems related to
aggression and agitation [52]. Aggression toward others and agitation are not equivalent to SIB on any
obvious dimension except, perhaps, exertion, and the fact that opiate blockers were ineffective in the
control of these behaviors adds inferential support to the argument that the opioid system is uniquely
implicated in SIB and not in other maladaptive behaviors. The effects of opiate blockers in children
who self-injure may be similar to the effects observed in adults but there are too few reports to make
that conclusion.
More recently, a thorough review of the scientific literature employing stringent and appropriate
criteria for inclusion concluded that the effects of opiate blockers on SIB could be evaluated in a total
of 86 patients [53]. Eighty percent of the subjects were reported to improve relative to baseline
(i.e., SIB reduced) during naltrexone administration. Of the subjects who improved, 47% exhibited a
reduction in SIB by 50% or greater. In studies reporting dose levels in milligrams, males were more likely than females to respond. No significant relations were found between treatment outcomes and
autism status or form of self-injury.
Two relatively large, placebo-controlled studies [16,54] included in this review of naltrexone came to
very similar conclusions. In a double-blind, placebo-controlled, dose-finding study, Sandman et al. [54]
reported that 18 of 21 individuals exhibiting SIB responded favorably to at least one dose (range of
0.5–2.0 mg/kg) of naltrexone (time-sampled video records provided direct observations of the subjects).
Acute treatment (1 week at each of three doses) with naltrexone reduced the frequency of SIB without
major side-effects. Activity, stereotypy, involuntary movement, and neurological status were not
influenced by naltrexone. There were two central findings. First, the highest dose (2 mg/kg) was the most
effective, confirming earlier results in this population [55,56]. Seven of the eight patients responding best
at the highest dose, also responded favorably to the 1 mg/kg dose. Six of these eight patients also
responded at the 0.5 mg/kg dose. Eleven subjects responded positively to both the 1 and 2 mg/kg doses.
Second, subjects with the most frequent SIB were the most positive responders to higher doses of
naltrexone, consistent with earlier reports [55,56]. A small minority of subjects responded most
favorably to lower doses. These results confirmed that at least 50% of the individuals with SIB
responded favorably to treatment with opiate blockers.
Another double-blind, placebo-controlled, fixed-dose study of eight, severe to profoundly retarded
adults included in the review [16], reported that treatment with naltrexone reduced head hitting, head
banging, and self-biting. The eight individuals evaluated displayed 18 forms of SIB. Improvement was
observed in 77% of the head hitting and head banging episodes and 100% of the self-biting forms.
Episodes of high frequency SIB also were more sensitive to treatment with naltrexone. The 100-mg
(high) dose was more effective than the 50-mg (low) dose in reducing SIB. For several individuals,
some forms of SIB decreased after naltrexone (e.g., head hitting and self-biting) but other forms
(e.g., throat poking) did not change. Four of the subjects in this trial received concomitant treatment
with clonidine (alpha-2-adrenergic agonist) but no effects on SIB or interactions with naltrexone were
observed. These findings compliment previous studies and caution that although naltrexone is effective
in reducing SIB, not all forms of self-inflicted harm may be controlled by blocking the opioid system.
These two relatively large studies of acute treatment with naltrexone came to very similar
conclusions. Opiate blockers appear to be an effective treatment for a significant number of individuals
exhibiting SIB. Administration of naltrexone reduces high frequency SIB and some, but not all, selfdestructive
behavior. Both studies acknowledged that not all individuals expressing SIB were positive
responders and that a small minority may increase SIB (see also Barrett [57]).
In the single study that has evaluated the effects of naltrexone using time-series analysis,
Symons et al. [58] made very interesting observations. First, they reported that three of the four patients
evaluated had at least a 33% reduction in their SIB. (The fourth patient had a 17% reduction in SIB.)
Second, and most interesting, they discovered that in addition to the improvement with naltrexone,
there was an alteration in the sequential dependencies between staff behavior and the manifestation of
SIB. During treatment with naltrexone, there was a significant increase in the probability that staff
would “prompt” individuals proximal in time and sequence to an SIB event for three of the four
patients, and a significant decrease in the fourth. One possible conclusion from these findings is that
naltrexone exerts its effects on SIB, in part by the opioid-mediated reinforcing influences of social
interactions. Alternatively, Symons et al. [58] suggest that SIB may be “multiply determined such that
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naltrexone may diminish opiate-mediated SIB leaving socially mediated SIB unchanged.” The overall
clinical implication is that many cases of SIB may be subserved by both opiate- and socially mediated
processes and that effective treatment for such cases would require a combination of naltrexone with
behavioral intervention strategies.
3.2. Long-Term Effects of Naltrexone Treatments
The long-term effects and consequences of continued treatment with naltrexone is not completely
known because most studies reporting treatment of individuals with SIB have been short-term
demonstrations or acute trials. Most published long-term studies have been either case studies or openlabel
designs and they have generated mixed results. Two types of studies comprise the long-term
evaluations of naltrexone, either prolonged treatment with naltrexone or extended observations
following brief periods of treatment. With these procedures, investigators have reported that about six
of eight patients examined in several studies exhibited long-term benefits in varying degrees from
treatment with naltrexone [57-59]. In the first report, a total of 24 days of naltrexone treatment resulted
in elimination of SIB in a 12-year-old girl that persisted for at least 22 months [57]. A similar finding
was reported after 1 year of continuous treatment with naltrexone in a 28-year-old woman with severe
SIB. Not only did treatment eliminate SIB but also the near-zero rate persisted through placebo and nodrug
phases of the study [59]. In their retrospective study of 56 patients, Casner et al. [60] discovered
that 57% of their patients treated with naltrexone between 3 and 878 months were considered to be
positive responders and 25% of these met objective criteria as responders.
We [61] examined the long-term (12 month) effects following acute treatment with naltrexone and
then we assessed the effects of subsequent long-term treatment with naltrexone. To accomplish this,
we enrolled 15 subjects in a double-blind, placebo-controlled acute dose-finding study. Each acute
dose was evaluated for a 1-week period with placebo weeks interspersed. Subjects were followed for a
12-month period and then they were enrolled in a multiple baseline design with a single most effective
dose (determined in the acute phase) administered to each subject for 2-, 3-month periods over an 18-
month interval with placebo periods appropriately separating the treatment phases. Again, timesampled
video records were scored using a computer-assisted program [62].
The primary finding from our study was that a subgroup of patients exhibited persisting effects
(decreased SIB) in the 12 months after acute treatment with naltrexone. Seven patients exhibited
decreased SIB over the 12-month period and five of these had a 75% reduction in SIB compared to the
placebo control period. These five patients, each with at least a 75% reduction in SIB, increased their
SIB when administered naltrexone in the long-term treatment protocol. The largest decrease in SIB was
observed in patients who had a brief exposure to naltrexone, were given a 12-month hiatus during which
they showed an increase in SIB, and then were readministered naltrexone several times in the 18-month
double-blind, placebo-controlled study.
4. Endogenous Opioid Levels Predict Response to Opiate Blockers
In our initial study to examine the relation between circulating endogenous opioids and response to
naltrexone, we collected blood samples from ten patients within 2–5 min of a self-injuring act and
during a control period [18]. At least 1 month later patients were administered three different doses of naltrexone in a double-blind, placebo-controlled crossover study over a 10-week period. All patients
were videotaped during the study and behavior was coded with a computer-assisted program. Patients
with the highest change in plasma levels of BE after SIB had the most and statistically significant
positive response to naltrexone. These results were consistent with several other reports. First,
Ernst et al. [21] reported that baseline levels of BE were positively related to changes in behavior
(clinical global impressions, CGI) after treatment with naltrexone in five young autistic children.
Second, Bouvard et al. [38] found that C-terminal BE decreased after naltrexone only in good
responders. Third, Scifo et al. [63] found that increases in SIB and response to naltrexone in some
patients, were related to high levels of endogenous opiates (i.e., good responses to naltrexone were
observed in patients with high levels of BE). Fourth, Cazzullo et al. [64] reported that patients
responding with decreased BE levels after treatment with naltrexone had better and more pervasive
behavioral improvement than patients who did not have physiological changes after naltrexone.
In a follow-up study of nine additional patients (total of nineteen), we [3] found that plasma BE was
uncoupled from the usually coreleased ACTH [65-71] after an episode of SIB. This unusual pattern was
not a function of time of day that blood was sampled, and it confirmed our earlier observations [7,18]
and provided additional support for this specific biological marker among a diverse group of subjects
who share a behavioral aberration. In addition, stronger support was generated for the effectiveness of
naltrexone in reducing SIB.
Positive responses to low doses of naltrexone were observed in subjects who did not exhibit
increased BE after SIB. That is, low doses of naltrexone were effective in reducing SIB only in
subjects either who did not exhibit a surge in BE after SIB or whose baseline level exceeded the level
after SIB. The relation between BE and response to the lowest dose of naltrexone was consistent with
our earlier results, and statistically significant with the addition of nine subjects. Previously we [3] suggested
that SIB had functional significance because it increased endogenous opiates and thereby
delivered positive consequences (i.e., pleasure/euphoria/pain modulation). We argued that the highest
dose of naltrexone most effectively blocked this mechanism in subjects with the highest levels of BE
after SIB. The results from the follow-up study suggested an alternative possibility related to baseline
levels of, or baseline relations between, POMC peptides. Because the lowest dose of naltrexone was
most effective in subjects with the highest (morning) baseline (relative to post-SIB) levels, we
speculated that the association between baseline ACTH and BE could influence the response to
naltrexone (based on evidence that supported reciprocal functions of BE and ACTH [72]]. If our
speculations were accurate, subjects with the greatest difference between morning BE and ACTH
levels would be the most responsive to low doses of naltrexone because there would be less attenuation
of the opioid influence. The test of this possibility confirmed our speculations because we found that
subjects with high levels of morning (chronic) BE and low levels of ACTH were associated with positive
responses to the low dose of naltrexone. This possibility may be compatible with findings that chronic
exposure to opioids resulted in supersensitivity to the effects of low doses of opiate antagonists [73,74].
These findings have since been extended using a fundamentally different method for quantifying
changes in the temporal patterning of SIB following treatment with naltrexone. The THEME method
developed by Magnusson [75,76] has been used to detect highly significant, nonrandom, hierarchical
patterns in the temporal organization of SIB with respect to other observed behaviors. Kemp et al. [10]
reported that these temporal patterns (“T-patterns”) of SIB were significantly correlated with basal
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levels of BE. In the subgroup of subjects receiving naltrexone (discussed above), the percent change in
these T-patterns of SIB (between weeks the subjects were receiving placebo and weeks they were
receiving naltrexone) was found to be significantly correlated with post-SIB (i.e., samples were
collected immediately after SIB) levels of the N-terminal fragment of beta-endorphin (βEN). No such
correlations were found for changes from placebo on any “control” T-patterns (those containing noninjurious,
stereotyped behaviors or staff interactions) nor for any samples collected during other
periods. These results are shown in Table 1.
Table 1. Pearson’s r coefficients (significance) between levels of beta-endorphin (Nterminal)
collected in either the AM, PM, or following SIB, no SIB, or physical exercise
(PE) and the change in the percentages of T-patterns (by behavior type) for weeks treated
with placebo and naltrexone.
We have made similar observations in our long-term studies of naltrexone and SIB [19]. POMC
fragments were measured in twelve self-injurious patients before and after long-term (3-month)
treatment with naltrexone. POMC fragments were sampled from blood collected at the end of the
baseline and placebo-controlled treatment phases of the study. Two patterns emerged. One group
(responders) displayed persisting improvement in SIB and lower relative levels of BE after initial
exposure to naltrexone. Chronic administration of naltrexone to this group was associated with
increased SIB and elevated relative levels of BE. Return to placebo improved their behavior (reduced
SIB) and their levels of BE returned to basal levels. The second group (nonresponders) was
characterized by absence of persisting improvement after acute treatment with naltrexone and by
elevated basal BE levels. Chronic treatment with naltrexone improved their behavior but did not alter
their BE levels. Long-term positive responders to acute doses of naltrexone were associated with less
disregulation of ACTH and BE.
5. Conclusions
When it was established that the body had its own opiate system [77], the endogenous opiates
became prime suspects responsible for maintaining SIB. Perhaps individuals who self-injure have
elevated thresholds for pain or derive pleasure from painful stimulation. Exposure to, or levels of,
endogenous opiates could explain these possibilities. Reduction in SIB following treatment with opiate
blockers would provide evidence for the opiate hypothesis of self-injury. Results from studies to test
these possibilities, however, are complex. The complexity is related primarily to the fact that patients
exhibiting SIB and evaluated after treatment comprise a mixture of etiologies, pathologies, and
motivations. Despite the tremendous amount of error introduced with a heterogeneous population,
there is substantial evidence that opiate blockers are efficacious in reducing SIB.
Beta-Endorphin (N-terminal) Levels
Change in T-Pattern % by Type: AM PM Post-SIB No-SIB Post-PE
SIB 0.37 (0.47) 0.25 (0.64) 0.82 (0.04) −0.45 (0.44) 0.66 (0.22)
Stereotypy −0.76 (0.07) −0.26 (0.96) 0.52 (0.29) −0.29 (0.64) −0.10 (0.87)
Staff Interactions 0.42 (0.41) 0.54 (0.27) 0.35 (0.49) −0.63 (0.25) 0.26 (0.68)
The observations that opiate blockers reduce SIB are important for at least two reasons. First,
naltrexone produces a clinically significant reduction in a serious and life-threatening behavior for
some individuals typically who have not been responsive to any other type of treatment. We have
observed startling improvements in individuals who have failed all rational treatments. Some adults in
our studies have had protective headgear discontinued for the first time since early childhood. Others
have developed adaptive skills and have acquired the ability (or the privilege) to leave institutions for
the first time in their lives after treatment with naltrexone. Second, the results with naltrexone are
important because they suggest that a specific biological system may be disregulated in a subgroup of
patients. Because the opiate blockers have few effects in the absence of opiates [78], effective
treatment with these drugs must engage the endogenous opioid system. Reports that resting levels of
endogenous opiates or levels of endorphin after an SIB episode predict positive responses to opiate
blockers provide support for this assumption and the foundation for rational treatment strategies based
on biological criteria.
From the current review we can draw several conclusions. There is consensus in the literature that
doses between 1.0 and 2.0 mg/kg or a fixed dose of 100 mg are the most effective for reducing
SIB [16,53,54]. At these doses, at least half of the chronically self-injuring patients exhibit at least a
25% reduction in their behavior. It is important to acknowledge that the studies that have reported
reductions of 25% or greater, typically conducted direct observations of the patients and did not rely on
global clinical ratings. As reviewed by Symons et al. [53], male patients respond more favorably to
naltrexone treatment than do female patients. There is consensus that naltrexone is a safe drug without
major or contraindicating side effects. Most individuals entered into naltrexone trials exhibited the
most severe SIB for which all other forms of treatment had been ineffective. Often their behavior
presented life-threatening consequences and always their SIB prevented them from enjoying a less
restrictive environment. Against this background, the possible benefits of reduced SIB by treatment
with naltrexone exceed the risk of side-effects. We are aware of clinical decisions to treat SIB with
naltrexone even when patients presented with risk factors such as chronic hepatitis [79]. To our
knowledge, there have not been serious side effects solely due to administration of naltrexone among
MR/NDD patients. There is consensus among the studies that naltrexone is an effective treatment
because the endogenous opioid system is engaged by SIB [3,16,18,19,57]. SIB has characteristics that
resemble addictive behavior (compulsive, ritualistic, destructive) and altered pain threshold. Both of
these characteristics implicate the opioid system and support the logic of opiate blockers as reasonable
treatments. There is consensus that long-term treatment of SIB with naltrexone apparently is not
harmful and may be effective. There is consensus that generally, treatment with naltrexone appears to
be effective in about half of the adult patients examined. Following effective acute treatment with
naltrexone some patients have shown a rebound to pre-treatment levels [61]. There is consensus that
naltrexone should be avoided during periods when patients are known to be in pain requiring narcotic
analgesics, such as surgeries or with bone fractures. Alternately, nonnarcotic analgesics should be
administered to patients receiving naltrexone [80]. Finally, it should be noted that there are reports of
paradoxical increases of SIB following treatment with naltrexone [81]. In our own research [61], we
have observed increased rates of SIB in individuals who showed sustained improvements throughout a
12-month hiatus following a brief period of acute treatment with naltrexone, and then were given longterm
treatment (3 month) with naltrexone.
Acknowledgements
This research was supported by award HD-48947 from the National Institute of Child Health and
Human Development. The assistance of Mohammed Lenjavi and Paul Touchette is gratefully
acknowledged.
Source with References;http://www.mdpi.com/1424-8247/4/2/366/pdf
(Reuters) – In her one-room flat, as a small shelf of porcelain cats looks on and the smell of mold hangs in the air, Zoya pulls down the left shoulder of her black blouse and readies herself for her next hit.
A friend and ex-addict uses a lighter to heat a dark, pebble-like lump of Afghan heroin in a tiny glass jar, mixes it with filtered water and injects it into Zoya’s shoulder. The 44-year-old widow is a wreck: HIV-positive, overweight and diabetic. After 12 years of dealing and drug abuse, the veins in her forearms and feet are covered in bloody scabs and abscesses, too weak and sore to take fresh injections.
Crimson-dyed hair frames her bloated face, which is made up to match a hot pink manicure. As the syrupy brown mixture enters her system, Zoya’s eyes glass over and she ponders her fate and that of her country.
„There are a lot of us. What do they (the government) want to do? Kill us?“ she says. „They want to gather us together and drown us? I worry for tomorrow’s generation.“
If Zoya is anything to go by, today’s Russians are hardly flourishing. Russia has one of the world’s biggest heroin problems, with up to three million addicts according to local non-governmental organizations. Twenty one percent of the 375 tons of heroin produced from Afghanistan’s opium fields now finds its way through central Asia into Russia, according the United Nations. (By contrast, China, with nine times more people, consumes just 13 percent.) The Russian government estimates its citizens bought $17 billion worth of street-traded heroin last year — about seven billion doses. The addiction kills at least 30,000 Russians a year, which is a third of the world’s total heroin-related deaths, adding to pressures on the country’s already shrinking population.
So grave is the problem that President Dmitry Medvedev last year branded heroin a threat to national security.
That’s one reason why last October, 21 years after the end of the decade-long Soviet war in Afghanistan, Russian troops joined forces with U.S. soldiers for a joint drug raid on four Afghan labs. The operation, which destroyed nearly a ton of heroin, was hailed a success and the Cold War foes said they would like to see more such operations in Afghanistan, which is responsible for 90 percent of the world’s heroin production.
At home, though, Russia has been far less active in tackling the problem. Critics go as far as to accuse Moscow of wilfully neglecting its citizens and thereby fuelling what the World Health Organization says is one of the fastest growing HIV/AIDS epidemics in the world.
Unlike most countries around the world, Russia refuses to finance harm reduction programs such as needle exchanges, or to legalize methadone. Over the past few months, Moscow has decided to discontinue the work of foreign donors and NGOs with heroin addicts. It even recently blamed foreign groups for worsening the country’s HIV epidemic.
Health experts and drug addicts alike point to official inaction as the real culprit. It’s as if Moscow has misinterpreted the old U.S. anti-drugs slogan „Just Say No“ and turned its back on the crisis. „My government does nothing for me. I am no longer a person in this society,“ says Zoya, who lives in Tver, a drab city of half a million just off the Moscow-St Petersburg highway, and whose husband, also an addict, died from AIDS several years ago.
Anya Sarang from the Andrey Rylkov Foundation for Health and Social Justice, a small UN-funded Russian organization set up in June 2009, says Russia is failing its people. „For the main groups prone to the disease — drug users, sex workers, migrants — there is absolutely nothing for them,“ says Sarang.
THE PROUD BEAR
Russian officials have a long history of denying crises. From the Soviet government’s refusal to help during the famine of the 1920s to its delay in responding to the 1986 Chernobyl nuclear accident, responses from the top have often mixed disregard and cover-up. During last August’s heat wave, as peat fires and acrid smoke killed hundreds, officials kept silent on the wider health effects of the smoke for weeks.
One of the reasons for the rush to denial lies in the national psyche. Russia is a deeply patriotic country, with a long history of strong governments far removed from the everyday concerns of ordinary citizens. After the humiliating collapse of the Soviet Union 20 years ago and the calamity and poverty that followed, the strongman rule of Vladimir Putin (former president and current Prime Minister) has allowed the Russian bear to flex its muscles on the international stage again.
But while Moscow crows about hosting such high-profile sporting events as the Winter Olympics and soccer World Cup, it ignores daily reality, says health worker Sarang. „Russia is trying to preserve a certain political image, showing that everything is fine,“ she says. „This has shown to be nothing more than a lie.“
Most Russians see the truth all around them. Zoya’s story is repeated so often across the country’s nine time zones that the reality is hard to ignore. Even the government estimates there are 1.8 million heroin users; activists and doctors put the number closer to 3 million, and in a study last June, the United Nations put it at 2.34 million or 1.64 percent of Russia’s population. That’s the world’s third highest heroin abuse rate in per capita terms after Afghanistan and Iran. In absolute numbers, the UN says, Russia is number one.
Heroin was virtually unheard-of during the Soviet era, but is now easy to buy in any city in the country. In Tver, a medium-sized city with relatively little industry and few job prospects for the young, the detritus of addiction — used syringes, needles — litters the streets. Deals are a regular sight on street corners.
Russia’s anti-drugs tsar, Viktor Ivanov, who heads the Federal Drug Control Service — a powerful government body given to U.S.-style rhetoric about the ‚War on Drugs‘– blames the country’s porous Central Asian borders for the heroin hunger.
„Unfortunately, in 1991 we suddenly found ourselves without borders,“ Ivanov told reporters in December, referring to the collapse of the Soviet Union.
Ex-Soviet Tajikistan, which borders Afghanistan and is one of the world’s poorest countries, has long been a haven for drug smuggling out of Afghanistan, where the Tajiks have ethnic ties. From there the heroin flows through Kyrgyzstan and Kazakhstan and into Russia.
INTERTWINED WITH AIDS
The drug problem has now become an AIDS problem. Officially, Russia has 520,000 registered HIV-positive people. The UN and local NGOs say there are probably closer to a million, maybe even more. HIV/AIDS has spread rapidly over the past decade, especially among drug users who regularly share dirty needles. The government estimates around a third of all drug users in Russia are HIV-positive; and international and Russian health experts worry the disease is beginning to spread to the general population through heterosexual sex.
The biggest problem, say health experts, is the government’s refusal to address Russia’s drug addiction. The lack of official intervention is remarkable. There are currently just 70 needle exchange and distribution programs in Russia, reaching a mere 7 percent of heroin addicts according to the London-based International Harm Reduction Association (IHRA). In terms of needle exchanges, „Russia is not even scratching the surface,“ says Rick Lines, executive director of the IHRA.
All the programs are run with foreign funding. Government support: nil. It’s not as if the government is powerless. In the one area of the HIV/AIDS epidemic where it is active — mother-to-child transmission — it has reduced transmission rates to almost zero.
HIGHWAY AIDS TEST
In the face of government inaction, grassroots groups have mushroomed across the country.
Outside Tver, Yuri Suring parks his beat-up black Toyota at a truck stop along the Moscow-Saint Petersburg highway every night. There, between 7 pm and 4 am, he surreptitiously doles out clean needles and condoms to prostitutes, many of whom work to support their drug addictions. „If I were not here, where would these girls go? Who would help them? No one,“ Surin says as a trio of prostitutes in knee-high boots and bomber jackets approaches the car.
Surin’s organization, We And AIDS, consists of himself, a second outreach worker and a driver. The supplies he hands out every night and the kits he uses to test women come, he says, from sympathetic doctors and western groups who want to help.
On a cold night in November, 20-year-old prostitute Olga slips into Surin’s car for an AIDS test. Surin rubs a two-inch indicator on her gums and inserts it into a small plastic tray while Olga nervously smokes a cigarette and shakes her black-bobbed head from side to side in anger at her fate, her gold leaf-shaped earrings swaying.
After studying the result — negative — the prostitute flings the indicator out of the car window and then hops across the gravel into a truck cabin where customers — two large middle-aged truckers — are waiting.
The Health Ministry says it spent 10 billion roubles ($320.5 million) on HIV/AIDS testing and treatment — mostly antiretroviral drugs — in 2010. But activists and health experts say this amount compares badly with other countries in the G20 and sufferers are routinely ignored.
In a 2010 report, the World Health Organization said just a fifth of Russians who needed AIDS drugs were receiving them. South Africa, which has the biggest HIV-positive population in the world — and whose government until recently was criticised as being in denial on AIDS — gives AIDS drugs at almost twice that rate.
„Appeals, trials and public action — nothing works,“ says Alexandra Volgina, head of The Candle Foundation for HIV-positive people, a non-governmental organisationorganization in Saint Petersburg.
When asked why so many sick Russians lack access to AIDS drugs, the health ministry’s spokesman responds: „The amount spent was deemed sufficient.“
POPULATION PROBLEMS
Russians usually blame alcohol for their health problems. Official data shows the average Russian drinks 18 liters (38 pints) of pure alcohol every year, compared with 14 liters in France and eight in the United States.
Official campaigns against drinking have been pursued sporadically since Tsarist times, usually with little success. In September last year Russia banned night-time sales of heavy alcohol, following on from a proposal to double the minimum price of vodka over the next two years in an effort to curb drinking.
„They (the government) are nicer to alcoholics than they are to us,“ says 32-year-old heroin addict and Tver resident Valera, whose scaly hands and face are covered in bright pink scabs from a decade of use. Like many drug addicts, Valera does not work and refuses to say how he funds his $300-a-day habit.
The Geneva-based International Aids Society Aids Society (IAS) warns that if Moscow continues to take no measures, the number of new HIV infections in Russia is likely to grow by 5-10 percent a year, pushing the problem to „an endemic level“, according to IAS president Elly Katabira: the rate will stay constant even without any additional infections from outside the country.
That would hit Russia’s already dwindling population — recently called a „demographic crisis“ by President Medvedev. Heavy smoking, alcoholism, pollution, poverty, low birth rates in the years after the fall of Communism, as well as HIV/AIDS underpin UN projections that the population will shrink to 116 million by 2050 from 142 million now. Moscow — which now gives money to mothers bearing two or more children – targets a population of around 145 million by 2025, but concedes that it could fall to as low as 127 million by 2031.
DESPERATE FOR METHADONE
If one thing appals foreign health officials and activists more than anythappallsing else about Moscow’s response to its heroin problem, it’s the ban on methadone. The WHO regards methadone as essential in combating heroin dependence, but in Russia anyone caught using it or distributing it can face up to 20 years in prison — as harsh a sentence as that for heroin.
Called a replacement drug, methadone is taken by mouth — so reduces the risk of HIV infection by using shared needles — and is used around the world to treat opiate addiction. Russia is one of just three countries in Eastern Europe and Central Asia to ban the drug, alongside Turkmenistan and Uzbekistan, where heroin consumption is relatively low. China, which has over one million registered heroin addicts, with unofficial estimates running several times that, has more than 680 methadone sites.
Methadone is a potent synthetic opiate in its own right, but it can eliminate the agonizing withdrawal symptoms that addicts experience when they quit heroin. Its main advantages are that it has to come from a health-care source, in controlled doses and without needles. That gives addicts some chance, over months or sometimes years, to go clean for good.
In Tver, Yuri Ivanov, a doctor and the deputy head of the state-run Tver Regional Narcology Clinic, is dumbfounded by the ban. „Why do civil servants limit me from doing my work?“ he asks in his dimly lit office in the crumbling grey clinic, which sits off an unpaved muddy lane in the center of the city. „All that they are trying to do is the opposite of what we need. It is hard for me to understand… The situation is going backward. When there is no real medicine, they go right back to drugs.“
Ivanov sometimes resorts to giving his patients tropicamide, a drug used by eye surgeons to dilate the pupils and which has a similar effect to heroin.
Addicts talk of their rare encounters with methadone users with a sense of wonder and even magic. „All of us know about this drug methadone and all of us want it. People come through who have done it and we can instantly see how much brighter and better they live,“ says Tver addict Valera in jittery sentences, high after shooting up twice by midday, in an interview in the back of his tobacco-stained car.
But Moscow won’t be swayed. „The medicine has become more dangerous than the illness. It would be replacing one evil with another,“ said the anti-drugs baron Ivanov. „And why on earth would we do that?“ Gennady Onischenko, the country’s top doctor, repeatedly dismisses methadone as „still a narcotic“.
In a major government anti-drug strategy launched last June, there was no mention of substitution therapy, even though Moscow says it is now focused on reducing the demand for drugs. That means that Russia’s measly four federal and 77 regional rehabilitation centers will continue to treat addicts with psychotherapy, counseling or simple painkillers.
CHAINED TO BED FRAMES
The vacuum created by the lack of effective substitution therapies was highlighted in an incident last October in the Ural Mountains town of Nizhny Tagil. Anti-drugs activist Yegor Bychkov, 23, was sentenced to three and a half years in prison for kidnapping drug addicts. Bychkov said he had received permission from the addicts‘ parents to forcibly take their sons and chain them to steel bed frames while they underwent a painful detox.
Anti-drugs chief Ivanov praised Bychkov, saying he had acted in good will; the head of the parliamentary health committee Olga Borzova said the state was to blame for his arrest as he had become desperate.
The Russian Orthodox Church also weighed in. Though its official stance is against sex education and it regards heroin use as a sin, it has set up its own rehabilitation centers which offer religious guidance. The Church also holds regular discussions with the UN over the HIV/AIDS crisis.
Unfortunately, those sorts of initiatives may be risky. Almost two years ago, the General Prosecutor’s Office was ordered by Russia’s Security Council to beef up prosecutorial measures against non-governmental organizations which advocate substitution therapy. Since then, activists distributing free needles have been detained on charges of aiding illegal drug use.
„Russian government officials consistently promote falsehoods about harm reduction, and deter those who speak in favor of them,“ the IHRA’s Rick Lines says. „Speaking honestly about the vast body of evidence supporting the effectiveness of methadone is a dangerous thing to do (in Russia).“
That may be why relations between the UN’s Global Fund to Fight AIDS, Tuberculosis and Malaria — which has been pushing for methadone legalization — and Russia’s health ministry ruptured at the end of last year. The Global Fund provides the most finance for HIV/AIDS prevention in Russia and granted $351 million to Russia for 2004-11. Now $16 million of that allocation remains, and is at risk of being cut this year.
Worse, say global health experts and local NGOs, is the health ministry’s decision to scrap the Global Fund’s needle distribution, HIV awareness and medication programs. „They proved ineffective and we shall not continue them after 2011,“ said Alexander Vlasov, the ministry’s spokesman.
In October, the health ministry directly accused the Global Fund of making the HIV epidemic worse. „In the regions where these (Global Fund needle) programs were operating, the spread of HIV infection increased three-fold,“ minister Tatyana Golikova told a narcology conference.
The Fund says it is keeping up a dialogue with the Health Ministry. But global health experts warn that the decision to end the Global Fund’s work in Russia will be catastrophic. „Russia will fall behind and lose the achievements made so far,“ warned IAS president Katabira. „We will not be able to recover the situation.“
Heroin and coffee. These two words come to mind when Lao Ta Saenlee, 74, smiles, gestures and chats while sipping Chinese tea at his newly-opened coffee shop in his village, Ban Huay Sarn, in Chiang Mai’s Mae Ai district. While coffee is his new-found passion, Lao Ta has long been infamous and associated with drugs and heroin trafficking in the North. Although it’s been three years since he was released from jail, a renewed passion for life still bubbles from every word as he talks about plans of starting a franchise of „Lao Ta Coffee“ shops across the North.
FROM JAIL TO JAVA: Left, Lao Ta Saenlee reflects on his life. Right, at the time of his arrest in 2003.
But he will never be able to dispel decades of accusations of drug trafficking _ an image attached to prominent former Kuomintang (KMT) fighters who fled southern China into Burma in 1949 before settling in the northern hills of Doi Mae Salong in Chiang Rai in the 1960s.
His name has been associated with the now deceased „Opium King“ Chang Chi-fu, or Khun Sa, and the current drug baron, Wei Hsueh-kang of the United Wa State Army. He knew them both but vehemently denies drug links with them.
FIRED UP: New Year at Lao Ta Saenlee’s home.
Lao Ta’s story is one of a boy soldier and young fighter whose life was moulded and shaped through the barrel of the gun. It ensured his survival during times of political upheaval and in the dense jungle along the border between Burma and northern Thailand during the Cold War.
Like other prominent former KMT fighters, his leadership qualities gained him armed supporters, but invariably living in a foreign land meant agreeing to be a pawn in Thailand’s fight against the communist insurgency from 1961-1982. He fought the insurgents in exchange for a place to live, and as a result his stature and influence grew. But like so many others who often lived and trod on the shadier side of life with frequent encounters with the law, he fell from grace and was imprisoned.
Now he’s back _ but it wasn’t easy.
During the height of the campaign against drugs by former prime minister Thaksin Shinawatra, police arrested and seized the property of thousands of suspects. About 2,500 were killed. In June, 2003, the authorities moved against Lao Ta.
“I remember that day well. It was 4 or 5am, and about 100 troops, cavalry and police surrounded my home and village. All entrances were blocked. They blocked the road leading to my home with a tank. They searched all the houses in the village. “They searched for two days but they didn’t find any drugs. They arrested some addicts and they confiscated a lot of weapons. But it’s normal for hilltribesmen to have weapons. The villagers need the weapons to defend themselves. There was a large quantity of weapons and ammunition in my home,“ he admits.
For the next four to five days, Lao Ta _ and two of his sons, Vijarn and Sukkasem, who were also arrested _ were flown to Chiang Rai and Chiang Mai for press conferences by authorities and then flown back home. “They wanted to make a big story out of my arrest,“ he recalled.
Lao Ta spent fours in jail (from 2003-2007) and faced four separate charges of illegal possession of 336g of heroin, trafficking in 400kg of heroin with intent to sell to Malaysia, hiring a gunman to murder a man in Chiang Mai’s Fang district and illegal possession of firearms and ammunition.
By 2007, the courts dismissed the drug trafficking and attempted murder charges because of insufficient evidence _ a result of conflicting testimony from prosecution witnesses. He was slapped with an 18-month jail term for illegal possession of firearms.
THE HILLS COME ALIVE: left to right, Lao Ta Saenlee enjoys New Year’s festivities at home.
Thaksin even suggested that Lao Ta’s defence capitalised on loopholes in the law and bribed his way out.
But while he was imprisoned, a sizeable chunk of Lao Ta’s cash _ “I don’t have millions I have only 76 million“ _ along with his properties, comprising a 300-rai lychee orchard, five houses in an up-market housing estate in Chiang Mai’s Muang district, and a supermarket in Ban Huay San, were seized by the government.
All that was left was his home, a petrol station and land that he acquired as payment for fighting the communists. The government could not seize the property because he and his family do not own it but have legally-issued documents allowing him and his to occupy and earn a living off the land.
“I had nothing left. My wife [he has three] had to sell 94 cows to live off while I was in jail. I could not even afford to buy pla too [mackerel] to eat,“ he insists. At one point when he was feeling depressed, Lao Ta actually considered robbing a bank. “I called up two of my most loyal supporters and suggested the idea. But they told me ‚Boss, we’re now 70 years old,“‘ he said, smiling. He admitted thinking about selling methamphetamines but dismissed the thought quickly.
Fortunately, he got a call from “a friend who used to traffic in drugs“ who congratulated him on his release and asked how he was doing. Lao Ta told him that he needed money to get his life back on track. “I told him I needed about six million baht. A few days later my friend put two million baht into my bank account. I tried to call and thank him but there was no answer and I have not heard from him since,“ said Lao Ta.
GONE STRAIGHT: Lao Ta Saenlee, now hopes to own a chain of successful coffee-shops.
Financially replenished and feeling better, old habits die hard. Lao Ta held a party in the village to mark his freedom. “We roasted pigs and had a grand party. I spent a lot.“ But reality set in and he had to think long-term. Ironically, he thought about Mao Zedong and Chiang Kai-shek. Both gave him the inspiration to move forward.
“In those days, both leaders headed countries that faced within insurmountable problems. They had nothing. But they both made something [their countries] out of nothing,“ he said.
Lao Ta still had his home and the land. But he also had notoriety _ a name people dhremembered, at least in the North. And so the idea of Lao Ta Coffee was born.
Lao Ta’s resilience probably did not stem from his thoughts of Mao Zedong and Chiang Kai-shek alone but because he’s had a life of struggle, depending on weapons to stay alive. Lao Ta says he “dragged a gun“ in Chiang Kai-shek’s army in southern China’s Yunnan province when he was just 13. In 1954, at 17, he joined remnants of the KMT’s 5th Regiment of the 93rd Division led by Gen Tuan Shi-wen into northern Burma. These forces fled Yunnan into Burma three years earlier and continued to fight against the forces of the new Chinese Communist regime.
In 1961, Lao Ta joined Gen Tuan and about 4,000 battle-weary KMT soldiers into Doi Mae Salong of Chiang Rai. In exchange for asylum in Thailand they fought Thai communist insurgents between 1961 to 1982. During this period they grew and sold opium to pay for their weapons. “At one stage the Thai government asked us to choose between leaving for Taiwan or staying behind. Many decided to leave for Taiwan. I recall looking at a map of the world to find out where Taiwan was. We could see that we had to travel a great distance across the sea. I was scared of the sea and feared I could never return home [to China]. So I decided to stay in Thailand and Khun Sa did toowas the same like us,“ Lao Ta recalled.
But his stay in Doi Mae Salong did not last long. He decided to move back into the Burmese jungles where he spent years trading in opium and building up his forces. “We grew up with guns and weapons and over time we [including Khun Sa] started building up our forces.“ Lao Ta said each individual leader built up their influence depending on the number of people loyal to them. He built up his followers from among the Muser, Lisu and Akha villagers.
“They spoke Chinese, so we could communicate with each other. You built up your position through your supporters and alliances with other groups. You needed this to survive. Opium was a commodity,“ he said. “I admit to having been a drug dealer,“ he said in an interview in June, 2003, before his arrest. “Back in the ’70s, in Doi Mae Salong, everyone did it. Opium was put in sacks and loaded onto helicopters. We didn’t have to take it to the market, buyers came to us.“ He also admitted to having “links“ to Khun Sa after he took control of the Doi Lang area in the early ’80s. In those days Lao Ta himself controlled 700-800 armed men.
Lao Ta was not clear as to when he returned to Thailand. But when he did, he was invited to work for the Thai military. The deal was simple _ Lao Ta and his men could keep their weapons. They were paid half a million baht and given 500 sacks of rice. In exchange, they would fight the communist insurgents. Once their mission was completed, they were promised Thai citizenship and land. They would not own the land, but he and his men _ and their families and descendants _ would have the right to live off it.
“I helped the Third Army fight the communists for many years. I was involved in no fewer than 200 operations,“ he said. Lao Ta and his men fought in Phayao, Nan and Phetchabun provinces and once were trucked to fight in the northeastern province of Loei. His military career ended in 1977, when aged 40, he was granted Thai citizenship and was allowed to live near Doi Mae Salong.
He settled in Tambon Ta Ton in Mae Ai district, and founded Ban Huay Sarn, the village where he lives now and which comprises 600 families and includes four smaller surrounding villages of 40-50 families each. He started growing cash crops and raised cattle obtained from Burma. But how does that explain the millions in cash and property he amassed in Chiang Mai by the time of his arrest in 2003?
Lao Ta admits that he knew Wei Hsueh-kang, the current drug baron, when Wei was based in Fang district of Chiang Mai before he joined Khun Sa at Ban Hin Taek in the Mae Chan district of Chiang Rai. When Khun Sa was forced out of Thailand, and as his influence waned, Lao Ta admits doing business with Wei when the United Wa State Army settled in Mong Yawn inside Burma near the San Ton Du checkpoint, which is close to his village. “The Wa needed supplies, food … everything,“ he said. Lao Ta adds however that he made “a great deal of money“ selling petrol to the Wa, especially when the Ban Ton Du checkpoint was closed. He paid bribes to get his 10,000 litre fuel trucks across into Burma. “But I was never involved in drug trafficking,“ he insists.
Over the years in Mae Ai district, Lao Ta’s influence grew, not only among villagers, but local government officials as well. He was involved in many community projects aimed at helping the villagers but he made sure he involved and worked closely with local officials and government agencies. He contributed openly and regularly to cash-strapped agencies. TVs, refrigerators and other office equipment at the local police station and district office bear the name of his other brother, Charan.
Although his relatives and close associates may have been arrested for drug trafficking, and Lao Ta had been involved in clashes with the law, before his arrest in 2003, Lao Ta was nominated twice as the best village headman in Mae Ai district. But ominous signs appeared on the horizon before his arrest _ the Chiang Mai governor dismissed him as village headman. Despite serving time, Lao Ta still enjoys widespread respect among the hilltribe villagers in the area who turned up in full force for their New Year celebrations at his home earlier this month.
The celebrations lasted three days and nights. There was singing and dancing. They lit firecrackers while village leaders fired their hand guns in the sky. “It’s a chance to clean the barrels of their pistols,“ quipped Lao Ta with a broad grin. Lao Ta provided the feast _ 30 pigs and 20 jars of home-made liquor.
The party was more joyful than it had been in previous years because Lao Ta was back to Ban Huay Sarn, the village he leads. And even though he’s now into coffee, his legacy continues _ his eldest son Vijarn, who served time with his father, is now the village headman.
source is: http://www.bangkokpost.com/news/investigation/218928/heroin-and-coffee—the-saga-of-lao-ta-saenlee
Bedeutungsinhalte und Konsummotive von Drogen haben sich in der Geschichte wechselseitig verändert. Das gilt auch für Substanzen, die heute unter dem Begriff hard drugs firmieren. Den Auftakt für deren weltweite Prohibition markierte die erste internationale Opiumkonvention von 1912. Gründe für dieses Abkommen sind zum einen im 19. Jahrhundert zu suchen. Die Briten intensivierten seit den 1820er Jahren den Opiumhandel mit China, der zwischen 1839 und 1860 in zwei Opiumkriege mündete, mit denen die Legalisierung des Opiums in China erzwungen wurde. Zum anderen tauchten in den um 1900 rasch wachsenden Städten der westlichen Welt Drogenkonsumenten auf, unter denen bestimmte Gruppen stigmatisiert bzw. als soziales Problem betrachtet wurden: so in den USA nicht etwa Morphinisten aus der Oberschicht, sondern Opium rauchende, chinesische Migranten und urbane Jugendgruppen, die unter anderem Heroin konsumierten. Unter dem Eindruck der Folgen des in China massenkonsumierten Opiums und der Angst vor einem expandierenden Drogenkonsum in der eigenen Gesellschaft formierte sich in den USA, Großbritannien und anderen europäischen Ländern im ausgehenden 19. Jahrhundert eine Anti-Opium-Bewegung, die auf ein globales Verbot von Opiaten, Kokain und später auch Cannabis hinarbeitete. Im Verlauf des 20. Jahrhunderts wurde das Prohibitionsregime zunehmend ausgebaut, was die Entstehung von hochprofitablen Schwarzmärkten förderte. Über Jahrzehnte konzentrierte sich die Bekämpfung des Drogenhandels auf repressive Maßnahmen und kulminierte seit den beginnenden 1970er Jahren im war on drugs. Wiederum wurden dabei nicht etwa Kokainkonsumenten aus wohlsituierten Kreisen problematisiert, sondern wegen ihrer Drogenabhängigkeit sozial gescheiterte Existenzen. Nicht zuletzt der Einsicht geschuldet, dass der Kurs dieser Prohibitionspolitik weitgehend kontraproduktiv war, sind seit einiger Zeit neue Ansätze erkennbar. Sie diffamieren Drogenkonsumenten nicht mehr als soziale Außenseiter, sondern setzen auf harm reduction. Dabei gewinnt auch die Erkenntnis an Boden, wie omnipräsent unterschiedlichste Drogen in unseren Gesellschaften sind und wie willkürlich die Grenzlinie zwischen legal und illegal in der Vergangenheit gezogen wurde.
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Im historischen Rückblick zeigt sich, dass das, was zu verschiedenen Zeiten und an verschiedenen Orten als „Droge“ definiert und begehrt oder gefürchtet wurde, äußerst veränderbar war. Psychoaktive Stoffe werden mit ganz unterschiedlichen Phänomenen und Problemen, mit denen sich Gesellschaften auseinanderzusetzen haben, in Verbindung gebracht. [1] In unserem Alltagsverständnis ist der Begriff „Droge“ zudem gespalten. Zum einen wird er im weitest möglichen Sinne verwendet. Weit davon entfernt, an Materialität gebunden zu sein, kann er sich auf alles und jedes beziehen, was über das normale Mittelmaß hinausreicht und den Menschen das Gefühl gibt, dass es über die Routinen des täglichen Lebens hinaus noch eine Welt gibt, in der Außerordentliches möglich ist und auch passiert.
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So analysiert etwa der Literaturwissenschaftler Peter von Matt das „Faktum“, dass die Geschichte einer Droge gleichkomme, die periodisch nationale Rauschzustände erzeuge, auf die dann der Cafard, die „graue Ernüchterung“, folge. Die „Intoxikation mit Heldenfabeln“ löse eine „gemeinschaftliche Erregung“ und eine „kollektive Anästhesie“ aus, die gegenüber den verübten Gewalttaten und dem Leiden der Opfer abstumpfe. [2] Das ist eine sehr weite Definition von Rauschdroge, die sich auch auf andere Ideologien und Betätigungen übertragen lässt, wie das Bergsteigen, die Sexualität oder das Spielen.
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Zum andern finden wir eine akute Engführung des Drogenbegriffs. Der Slogan „No drugs“ propagiert Abstinenz gegenüber jenen Substanzen, die im 19. Jahrhundert zu „Rauschgiften“ umdefiniert wurden, im Verlaufe des 20. Jahrhunderts auf die Liste der Betäubungsmittel gerieten und damit zunehmend in die Illegalität und auf Schwarzmärkte abgedrängt wurden. Drogen sind hier per definitionem jene Stoffe, die verboten sind. Die Promotoren der Prohibition erklärten immerzu, das Verbot sei nötig, weil diese Substanzen zu gefährlich seien. [3] Der umgekehrte Zusammenhang und auch die Tatsache, dass mit der Prohibitionspolitik bestimmte soziale Gruppen marginalisiert und Menschen stigmatisiert, wurden so wie damit überhaupt symbolische Gesellschaftspolitik betrieben wurde, sind hingegen kein Thema. Im Folgenden soll das Drama der Drogenprohibition im Zeitraffer so nüchtern wie möglich dargestellt werden.
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Schon in der Frühen Neuzeit wurden viele Stoffe, die im Zuge der kolonialen Expansion nach Europa kamen, als Gefahr für die soziale Ordnung wahrgenommen und verboten. Regierungen und religiöse Gewalten richteten sich vor allem gegen den Konsum von Tabak, Tee, Schokolade und Kaffee. [4] Von diesen Bestrebungen, Drogen zu unterdrücken, führt allerdings kein direkter Weg in die moderne Prohibitionspolitik, wie sie seit Ende des 19. Jahrhunderts aufkam und sich zunächst gegen das Opium richtete.
<5>
Die Anfänge dieser Verbote sind vielfältig und sie sind in internationalen Zusammenhängen ebenso zu finden wie in nationalen Kontexten und lokalen Problemlagen. Die beiden Opiumkriege der 1840er und 1850er Jahre [5], mit denen Großbritannien die Legalisierung des Opiums in China mit Waffengewalt erzwang, um das angeschlagene, jedoch noch immer einträgliche Geschäft mit diesem in Indien angebauten Stoff zu retten, stellten einen Ausgangspunkt für moralische Empörung und eine humanitäre und auch medizinisch inspirierte Rhetorik der Opium-Abolition in Europa und den USA dar. [6] Die Tatsache, dass die Briten am anderen Ende der Welt militärische Machtmittel einsetzten, um Profite aus „Rauschgift“ zu schlagen, weckte im entfernten Europa das Bewusstsein für die Universalität dieses Problems und mobilisierte Gegenkräfte, die sich nun mit moralischen, aber auch wirtschaftlichen Argumenten gegen diese imperialistische Politik zu wenden begannen. Damals entstand jene Problemsensibilisierung, die eine Anti-Opium-Stimmung provozierte, aus der sich anderthalb Jahrzehnte später eine organisierte Antiopiumbewegung formierte.
<6>
Bereits 1840 hatte in England eine sogenannte Anti-Opium-Society Informationsbulletins gegen die britische Kolonialpolitik publiziert. 1874 wurde die Anglo-Oriental Society for the Suppression of the Opium Trade (SSOT) gegründet, eine Vereinigung, die sich bald zur wichtigen Pressure group zur Unterdrückung des Opiumkonsums auch in England selbst entwickeln sollte und die zunehmend durch die Politik der amerikanischen Regierung unterstützt wurde. Aus einem „Nicht-Problem“, das mit einem Nicht-Wissen einherging, entwickelte sich so um die Mitte des 19. Jahrhunderts eine politisch-gesellschaftliche „Frage“, die „Opiumfrage“. Wenn einmal eine solche „Frage“ in der Arena der öffentlichen Meinungsbildung angekommen war, nahm die Besorgnis über diesen Missstand im gleichen Maße zu wie das Wissen darüber.
<7>
Der Weg zu einer rechtlichen Regulierung des ganzen Komplexes wurde somit durch den Imperialismus vorgespurt. Im Gravitationszentrum der Erschütterungen, die Opium in europäischen und amerikanischen Köpfen auslöste, befand sich China. Der ganze Ferne Osten wurde zur Drogenproblemzone und als entsprechend exotisch wurde das Phänomen wahrgenommen. Als 1909 eine Kommission die „Opiumfrage“ erstmals auf dem internationalen Parkett breit aufrollte, tagte sie in Shanghai. Federführend waren allerdings schon damals die USA, die unmittelbar im Anschluss an diese sogenannte Shanghaier Kommission mit der Vorbereitung einer ersten internationalen Opium-Konferenz begannen, die nun aber in Europa stattfinden sollte.
<8>
Am 1. Dezember 1911 wurde diese unter dem Vorsitz von Bischof Charles Brent im Haag eröffnet. Die zwölf teilnehmenden Länder – eingeladen waren 14, aber Österreich-Ungarn und die Türkei hatten abgesagt – tagten bis zum 23. Januar 1912 und verabschiedeten als Resultat der Verhandlungen die Erste Internationale Opium-Konvention von 1912, das Grundlagendokument der modernen Prohibitionspolitik. Diese Haager Opium-Konvention stellte allerdings keine rechtlich verbindlichen Verhaltensregeln, Anweisungen und Maßnahmen auf; sie gab bloß Empfehlungen. Dennoch war ihre Wirkung viel weitergehender, als dies aufgrund der juristisch schwachen Konstruktion angenommen werden konnte, gab sie doch die Richtung vor, entlang der nun nach und nach in (fast) allen Ländern nationale Drogengesetze erlassen wurden. Das internationale Abkommen wurde durch eine steigende Zahl von Staaten ratifiziert und begann, eine Breitenwirkung zu entfalten.
<9>
Die USA fungierten also – dies machte das Zustandekommen dieses ersten internationalen Opium-Abkommens deutlich – als spiritus rector bei der Genese des modernen War on drugs. Die Drogenprohibition kann jedoch nicht auf die Intentionen, Interessen und Präferenzen eines nationalen Akteurs zurückgeführt werden. Sie lässt sich nicht auf Strategien von mächtigen Staaten und „Moralunternehmern“ herrunterbrechen. Vielmehr gilt es, sie als entangled history zu verstehen, in der globale Austauschbeziehungen und eine ganze Reihe von Entwicklungen in der Gesellschaft, der Wirtschaft, der Wissenschaft und in den globalen Beziehungen zusammenwirkten. [7] Gegen Ende des 19. Jahrhunderts hatten sich offenbar politische Problemstellungen, mentale Dispositionen und massenmediale Ensembles aufgebaut, welche die öffentliche Resonanz für Verbotsargumente deutlich erhöht hatten. Es sind vor allem drei transnationale Entwicklungen, auf die hier hinzuweisen ist.
<10>
Erstens wurde die opiumfeindliche Haltung der USA von Anfang an in starkem Ausmaß durch rassische Gesichtspunkte und rassistische Motive bestimmt. [8] Die USA, ein Einwanderungsland par excellence, verstanden sich zwar als melting pot. Dennoch blieben ethnische Grenzziehungen virulent und einige von ihnen schlugen in offene Diskriminierung um. Nach 1850 begannen Chinesen in großer Zahl in die USA einzuwandern und viele von ihnen waren habituelle Tschandu-Raucher, wie die Pfeifen gebrauchenden Opiumkonsumenten genannt wurden. Die chinesischen Immigranten galten als äußerst leistungsfähige Arbeitskräfte, die in Bergwerken, in der Landwirtschaft, in Wäschereien und im Bau- und Transportsektor Beschäftigung fanden.
<11>
Insbesondere nach der Fertigstellung der großen transkontinentalen Eisenbahnlinien sahen die weißen (das heißt die europäischen) Amerikaner in den opiumrauchenden „Kulis“, die sich – unter anderem gerade wegen dieser Sitte – auf dem Arbeitsmarkt erfolgreich behaupteten, eine unwillkommene Arbeitsmarktkonkurrenz. Mittels einer „anti-orientalischen“ Kampagne wurde diese Minderheit nun zunehmend über ihre Droge stigmatisiert und unterdrückt. 1875 erließ die Stadt San Francisco die erste Strafnorm gegen Drogenkonsum in der westlichen Welt, und zwar ausschließlich gegen das Rauchopium der Chinesen. In der Folge wurde systematisch eine sogenannte „gelbe Gefahr“ heraufbeschworen: Phantastische Schilderungen von Opiumhöhlen, die in den Ausschmückungen von Moralaposteln alsbald zu reinen Inkarnationen aller kleinbürgerlichen Ängste, zu Orten der Unsittlichkeit und des physisch-psychischen Zerfalls gerieten, machten die Runde. Chinesen galten alsbald als ebenso gefährlich wie das Opium, das sie rauchten, und die „Höhlen“, in denen sie dies taten.
<12>
Unter diesen Umständen war der Gesetzgeber gefordert, der fortan zwischen der Unterdrückung des Opiums und der Diskriminierung der Chinesen oszillierte. Der Kongress wurde aktiv und beschloss 1887 ein Gesetz, das es den Chinesen, nicht aber den Amerikanern, untersagte, Opium zu importieren. 1889 richteten sich weitere Maßnahmen direkt gegen die Einwanderer: Der Chinese Exclusion Act schob der weiteren Einwanderung von ChinesInnen einen Riegel vor. 1890 stand dann wieder die Droge im Zentrum: Ein Gesetz behielt die Herstellung von Rauchopium exklusiv amerikanischen Staatsbürgern vor. 1909 schließlich wurde die Einfuhr von Rauchopium generell verboten. Es handelte sich hier um den ersten War on drugs, um einen amerikanischen Krieg gegen Opium und – da die Konnotation der Öffentlichkeit regelrecht eingehämmert wurde – gegen die in Amerika ansässigen Chinesen. [9]
<13>
Im heutigen Jargon könnte man von einer symbolischen Statusdegradierung einer ethnischen Minderheit durch Stigmatisierung einer Identität stiftenden, alltagskulturellen Droge sprechen. Eine herausragende Rolle spielte hierbei jener Flügel der amerikanischen Gewerkschaftsorganisationen, der sich voll auf die rassistische Rhetorik weißer Überlegenheit eingelassen hatte. Samuel Gompers (1850-1924), konservativer amerikanischer Gewerkschaftsführer, Kämpfer gegen sozialistische und anarchistische Strömungen innerhalb der Arbeiterbewegung und Mitbegründer der American Federation of Labor (AFL), deren Präsident er zwischen 1886 und 1924 war, machte den Schutz der teuren weißen gegen die billigen farbigen Arbeitskräfte zur gewerkschaftlichen Hauptforderung.
<14>
1902 veröffentlichte Gompers zusammen mit einem Co-Autor ein Pamphlet mit dem Titel: „Einige Gründe für die Fernhaltung der Chinesen: Fleisch oder Reis, amerikanische Männlichkeit oder asiatisches Kulitum, was soll überleben?“ Unter anderem ließ er verlauten: „Die überlegenen Weißen waren gezwungen, die minderwertigen Asiaten durch Gesetz oder, falls notwendig, durch Waffengewalt fernzuhalten (…). Die gelbe Rasse neigt von Natur aus zu Lüge, Betrug und Mord, und 99 von 100 Chinesen sind Glücksspieler“. Solche Haltungen können plausibel machen, weshalb die Unterdrückung des Opiums nicht beim Opiat Morphium, sondern bei der schonendsten Konsumform, beim Rauchopium einsetzte. Diese Geschichte aus den USA ist exemplarisch. Auch in andern Ländern gab es Bestrebungen, kulturelle Minderheiten über ihren Drogengebrauch zu definieren und sie mit einer Verbotspolitik zu bedrängen.
<15>
Zweitens zeichnete sich gegen Ende des 19. Jahrhunderts eine epochale Machtverschiebung ab. Mit ihrem Aufstieg zur neuen Hegemonialmacht im Pazifik, die 1898 mit dem Krieg gegen Spanien und der Eroberung der Philippinen einsetzte, erhielt der „symbolische Kreuzzug“ gegen das Opium erstmals eine globale Machtbasis. Dass nun die „Opiumfrage“, welche das britische Empire unter Zugzwang setzte, auf die Tagesordnung der internationalen Politik gesetzt wurde, resultierte auch aus der im ausgehenden 19. Jahrhundert sich verallgemeinernden Tendenz zu grenzüberschreitender Kooperation. Diese wurde angeregt durch neue weltumspannende Transport- und Kommunikationssysteme (Telegraphen- und Eisenbahnnetz, Hochseeschifffahrt). Und sie wurde nötig aufgrund der Vertiefung der internationalen Arbeitsteilung und einer zunehmenden Weltmarktverflechtung.
<16>
Derselbe Industrialisierungsschub, der über den Rüstungswettlauf die imperialistischen Rivalitäten zwischen den europäischen Großmächten steigerte und das internationale Spannungspotenzial erhöhte, setzte auch Impulse für eine transnationale Zusammenarbeit und eine assoziative Außenpolitik frei. Dabei war die Zunahme von internationalen Konferenzen, die sich „nichtpolitischer Fragen“ annahmen, charakteristisch. In deren Zentrum stand neben den technisch-infrastrukturellen Problemen und Standardisierungspostulaten vor allem der Schutz der Bevölkerung gegen einen befürchteten Sittenverfall. Neue technische Experten, professionelle Spezialisten und sachkundige Repräsentanten privater humanitärer Organisationen traten auf dem außenpolitischen Parkett auf und drängten die universaldilettantischen Diplomaten von altem Schrot und Korn in die Defensive. Die mit der „Opiumfrage“ befassten internationalen Konferenzen wären ohne diesen Trend zur „Versachlichung“ und ohne die Professionalisierung des Verhandlungsstils kaum zustande gekommen.
<17>
Die machtpolitischen Motive blieben jedoch weiterhin wirksam. So konstatierte zum Beispiel Albert Wissler in seiner 1931 veröffentlichten Basler Dissertation, „wie sehr die amerikanische Haltung in der Opiumfrage zusammenstimmt mit den weltwirtschaftlichen Interessen des Landes“. „Wie die christlichen Missionare bisher dem europäischen Kolonialimperialismus willkommene Vorarbeit geleistet haben, missioniert nun die amerikanische Moral – ebenso gutgläubig wie jene – für den amerikanischen Finanz- und Wirtschaftsimperialismus“, schrieb Wissler weiter und sah im „Missionsfanatismus der Amerikaner in der Opiumfrage“ eine „unschätzbare Waffe der amerikanischen Pazifikpolitik, der der alte europäische Kolonisator im Osten nichts Gleichwertiges entgegenzustellen hat.“ [10] Die moralisch sauberen Amerikaner im Kampf gegen die schmutzige Machtpolitik der alten, korrupten Kolonialmächte: Das war die Formel der neuen Prohibitionspolitik. [11]
<18>
Um die gesellschaftliche Neubewertung der „Drogen“ und die Ausweitung der Problemperzeption auf neue Stoffe, insbesondere auf Morphium, Heroin und Kokain zu erklären, ist es drittens nötig, die Veränderungen der Konsumentenstruktur und der Konsummuster zu analysieren. Die moderne Drogengesetzgebung war, wie gezeigt, mit einer Diffamierung „fremder Sitten“, mit der Ausgrenzung und Stigmatisierung von Minderheiten verbunden. In den USA richtete sich die Drogengesetzgebung bis ins 20. Jahrhundert hinein ausschließlich gegen Chinesen und ihre Droge „Rauchopium“.
<19>
Die Konsumentinnen und Konsumenten des weit stärker wirkenden, industriell hergestellten Morphiums hingegen wurden kaum als Problemfälle angesehen und deshalb noch bis zum Ersten Weltkrieg kaum behelligt. Zwar gab es auch in diesem Konsumsegment „einfache Leute“, insbesondere Kriegsveteranen, die während des Sezessionskrieges von 1861-65 verwundet und aufgrund der medikamentösen Behandlung mit Morphium von diesem Stoff abhängig geworden waren (oder ihn einfach schätzen gelernt hatten). Hier ging die Respektabilität der Suchtursache – Verwundung im Krieg – zusammen mit der Konformität der Süchtigen, die keinesfalls aufzufallen beabsichtigten, sondern in ihrer großen Mehrheit ein „ganz normales Leben“ führten.
<20>
Daneben wurde Morphium in Mittel- und Oberschichten, insbesondere auch in Ärztekreisen, gespritzt. Hierbei handelte es sich aber, wie die Untersuchung von Charles E. Terry und Mildred Pellens aus dem Jahre 1928 festhielt, um die „gebildetsten, anerkanntesten und nützlichsten Schichten der Gesellschaft“; in derselben Studie wurde die sogenannte „typische Konsumentin“ als eine „zarte Frau mit hellblauen Augen und flachsgelbem Haar“ geschildert. [12] Das war so ziemlich das Gegenbild zu den Chinesen; es gab also keine Anhaltspunkte, die ein Eingreifen im Milieu des Morphiumkonsums nötig gemacht hätten.
<21>
Schon vor dem Ersten Weltkrieg ereignete sich aber in den amerikanischen Großstädten eine dramatische Veränderung des Drogengebrauchs. Nun bildeten sich drogenzentrierte Subkulturen von Jugendlichen heraus. Dieselben Stoffe, die bisher in diskreter und medikalisierter Form appliziert wurden, gingen nun plötzlich mit marginalen Milieus, mit gescheiterten Individuen, kurz mit Problemen aller Art eine Verbindung ein. Das veränderte ihre Bewertung fundamental. David T. Courtwright zeigt in seiner die Opiumabhängigkeit in den USA behandelnden Untersuchung „Dark Paradise“, [13] dass die Zahl der Süchtigen zwischen der Jahrhundertwende und den 1940er Jahren insgesamt abnahm. Trotzdem führte die Anstiegstendenz in einem problematischen Sozialsegment zu einem drastischen Imageverlust der Stoffe und ihrer Konsumenten. Courtwright weist darauf hin, dass die mit der Drogenverfolgung befassten Instanzen auch mit irreführenden und gefälschten Statistiken operierten, um ihre Horrorvisionen plausibel zu machen.
<22>
Drogenkonsum wurde nun auch aus ärztlicher Sicht neu gedeutet. Wenn früher überhaupt eine Diagnose gestellt wurde, so lautete sie auf „moralische Schwäche“. Jetzt aber wurde das Problem verstärkt in Kategorien einer „mentalen Pathologie“ gefasst. Spätestens in den 1920er Jahren verfügte der durchschnittliche Doktor über die fixe Idee, bei Drogenkonsum handle es sich um ein psychopathisches Phänomen, die Betroffenen seien psychisch gespaltene, bewusstseinsgestörte, potenziell gefährliche Individuen, für die doch wohl eher Polizei und Justiz zuständig seien.
<23>
Ein repressiver, diskriminierender Hardline-approach begann sich durchzusetzen. Als „kriminelle Süchtige“, aber auch als „Geisteskranke“, wurden Drogenkonsumenten zunehmend marginalisiert, stigmatisiert, verfolgt. Wer diese Tendenz kritisierte, wurde der Schönrednerei bezichtigt und alternative Konzepte hatten keine Chance mehr angesichts der alarmierenden Rhetorik der „Rauschgiftgefahr“. Internierung und Kriminalisierung ersetzten für ein Dreivierteljahrhundert, das heißt bis ins ausgehende 20. Jahrhundert hinein, die bisherige Strategie einer diskreten Medikalisierung der Abhängigkeit.
<24>
Es wird im langen Zeitverlauf deutlich, dass sich Drogenpolitik kaum mit dem Interpretationsmuster der Humanitarian reform deuten lässt, wie das die frühere Geschichtsschreibung zu tun versuchte. [14] Die Geschichte der rechtlichen Regulierung des Problems muss vielmehr mit globaler Machtpolitik, mit gesellschaftlicher Normalisierung, mit Medikalisierungs- und Verwissenschaftlichungsprozessen sowie mit medialen Strategien erklärt werden. Was 1912 im Haag beschlossen wurde, war ein noch wenig gefestigtes Rahmenwerk. 1913 und 1914 fanden zwei weitere internationale Opiumkonferenzen im Haag statt.
<25>
Nach Abschluss der dritten Zusammenkunft im Dezember 1914 – die militärische Auseinandersetzung, die sich zum Ersten Weltkrieg ausdehnen sollte, hatte inzwischen begonnen – belief sich die Zahl der Staaten, die die Konvention unterzeichnet oder entsprechende verbindliche Erklärungen abgegeben hatten, auf 46. Das reichte aus, um das Abkommen endlich in Kraft zu setzen. Mit der Ratifikation, das heißt mit der Anpassung des innerstaatlichen Rechts an die völkerrechtlichen Normen, die mit dieser Sanktionierung durch die gesetzgebenden Körperschaften einzelner Länder überhaupt erst rechtsverbindlich und konkret anwendbar wurden, haperte es jedoch beträchtlich. Das sollte sich nach Kriegsende ändern. Das Haager Opiumabkommen wurde nämlich zum Bestandteil der Pariser Friedensverträge (darunter das „Versailler Abkommen“) von 1919/20 gemacht. Auf diese Weise wurde in allen Signatarmächten eine „automatische Ratifikation“ ausgelöst.
<26>
In Folge war es der 1919 gegründete Völkerbund, der für die Narkotika zuständig war und der weitere Konferenzen zur Betäubungsmittel- oder – wie es nun verstärkt hieß – zur Rauschgiftproblematik organisierte. 1924/25 fand in Genf eine weitere internationale Konferenz statt, in deren Vorfeld heftige Konflikte zwischen den beteiligten Staaten ausgetragen wurden. Das Epizentrum der Drogenproblematik hatte sich nämlich inzwischen in die europäischen Industrieländer verlagert. Im Verlaufe des Ersten Weltkrieges waren die symbiotischen Beziehungen zwischen Krieg und Droge noch enger geworden, als sie das seit dem Krimkrieg (1853-1856) und dem amerikanischen Sezessionskrieg (1861-1865) ohnehin schon waren.
<27>
Dabei spielten die zu Beginn des 19. Jahrhunderts entdeckten und fabrikmäßig produzierten Alkaloide – Morphium, sein Derivat Diacetylmorphin (Markenname „Heroin“) und Kokain – die Hauptrolle. Morphium ist bis heute eines der leistungsfähigsten, wenn nicht überhaupt das wirksamste Analgetikum; Kokain diente vielfach als Lokalanästhetikum, das heißt als Mittel zur lokalen Betäubung bei kleineren chirurgischen Eingriffen. Dass der Erste Weltkrieg den Bedarf an solchen Stoffen dermaßen stark steigern würde, war ursprünglich nicht abzusehen gewesen; es sollte ja ein kurzer Krieg werden – ähnlich dem deutsch-französischen Krieg (1870-1871).
<28>
Die Hochrüstung durchkreuzte diesmal die Strategie der schnellen Entscheidung. Ab 1915 erstarrte die militärische Auseinandersetzung im Grabenkrieg. Es kam zu langanhaltenden, mörderischen „Materialschlachten“, die erstmals mittels Giftgas, Maschinengewehren, Tanks, Flugzeugen et cetera geführt wurden. Über 65 Millionen Soldaten standen im Einsatz; die Verlustbilanz lautete: etwa 10 Millionen Tote, über 20 Millionen Verwundete. Der Bedarf an Alkaloiden stieg unter solchen Umständen natürlich enorm an; die chemische Industrie, die eben erst den Einstieg in die Pharmaproduktion geschafft hatte, konnte europaweit mit Hochkonjunktur rechnen. Es ist nachvollziehbar, dass die entsprechenden Unternehmen nach 1918, nach dem Wegfallen eines Teils der kriegsbedingten Nachfrage, nach neuen Absatzmärkten suchten und diese zum Teil in Kolonialgebieten – etwa in China, aber auch in Nordafrika – fanden.
<29>
Angesichts dieser Entwicklung lehnte es England ab, sich durch den Völkerbund an eine internationale Konferenz zitieren zu lassen, in der erneut und exklusiv das „alte“ koloniale Opiumproblem im Vordergrund gestanden hätte. London mobilisierte nun gegen die – wie sie von A. Wissler bezeichnet wurde – „mitteleuropäische Alkaloidindustrie“, das heißt vor allem gegen Deutschland und die Schweiz, aber auch andere Länder wie Frankreich, und wies darauf hin, dass mit der massenhaften Fabrikation von Alkaloiden ein neues Drogenproblem entstanden sei. So wurde denn beschlossen, zwei Konferenzen einzuberufen, von denen sich die eine mit der allmählichen Unterdrückung des Opiumgebrauchs im Fernen Osten und die andere mit der Beschränkung der Herstellung von Alkaloiden durch die Industrieländer befassen sollte. Aus dieser letzteren Konferenz resultierte das Genfer Abkommen, das in Folge durch eine große Anzahl von Ländern unterzeichnet und auch ratifiziert wurde.
<30>
Dieses Genfer Abkommen bedeutete allerdings eine Lockerung der 1912 formulierten Zielsetzungen, den Konsum von Betäubungsmitteln über eine strikte internationale Reglementierung von Produktion und Handel zu erzielen. Von einer rigorosen Kontingentierungslösung wurde im Interesse der chemisch-pharmazeutischen Unternehmen abgesehen; die Konferenzteilnehmer einigten sich auf ein ziemlich unverbindliches Zertifizierungssystem, das viele Umgehungsmöglichkeiten sowie Verhandlungsspielräume offen ließ und die Produktion von Morphium, Heroin und Kokain in Gang hielt.
<31>
In einem für den weiteren Gang der Drogendiskussion bedeutsamen Punkt verschärfte das Genfer Abkommen von 1925 allerdings die Prohibition: Cannabis, das 1912 zwar schon angesprochen, jedoch noch nicht explizit erwähnt wurde, geriet nun auf die Liste der inkriminierten Stoffe. [15] Daraufhin wurde vor allem diese Droge ins Visier der Prohibitionisten genommen. Auch hier profilierten sich die USA in einer Pionierrolle. Dies hing mit einer Kampagne gegen die Chicanos, die spanisch sprechende Bevölkerung des Südwestens der USA, die durch Einwanderer aus Mexiko Zuwachs erhielt, zusammen; es handelte sich hier um eine mit dem gegen die chinesischen Arbeitsimmigranten gerichteten Antiopiumfeldzug vergleichbare Tendenz zur Stigmatisierung einer ethnischen Minderheit, die sich ohne Probleme auch auf die Afroamerikaner ausweiten ließ. Erneut diente die Droge als Vehikel. Insbesondere in der Großen Depression der 1930er Jahre zog dieser Feldzug gegen Marihuana immer weitere Kreise; der Tonfall verschärfte sich, die Öffentlichkeit wurde über die Medien mit einer neuen, heimtückischen Bedrohung gigantischen Ausmaßes bekannt gemacht.
<32>
1930 nahm das Bureau of Narcotics seinen Betrieb auf; dieses betrieb die Dramatisierung der Drogen durchaus auch im bürokratischen Eigeninteresse. Nachdem Franklin D. Roosevelt nach seinem Amtsantritt 1933 die Alkoholprohibition aufhob, wurde ein Teil der Alkoholfahnder auf Cannabis angesetzt. Harry J. Anslinger, herausragender Exponent des Abwehrkampfes gegen Marihuana, Commissioner im Bureau of Narcotics, bearbeitete die Medien nach Strich und Faden.
<33>
Ein Beispiel: In einer von 56 Zeitungen nachgedruckten Meldung, die auf Materialien von Anslinger basierte, wurde unter dem Titel „Morde durch die Mörderdroge überfluten die USA“ verlautet: „Schockierende Gewaltverbrechen nehmen zu. Metzeleien, grausame Verstümmelungen, Verunstaltungen, kaltblütig durchgeführt, als würde ein hässliches Monstrum in unserem Lande umgehen. (…) Diejenigen, die süchtig nach Marihuana sind, verlieren nach einem anfänglichen Gefühl von Lustigkeit bald jegliche Hemmung. Sie werden zu bestialischen Dämonen, voll irrer Lust zu töten.“
<34>
Marihuana als „Killerdroge“: Hier taucht der ganze Assoziationskomplex der mittelalterlichen Assassinen wieder auf, hier wurde eine lange Tradition der kulturellen Degradierung des Orients auf die Spitze getrieben und mit einer Vielzahl von modernen Klischees zu einem furchtbaren Feindbild amalgamiert. [16] Die Kampagne war aus der Sicht des Bureau of Narcotics ein Erfolg, kam doch 1937 der Marihuana Tax Act zustande, der Cannabiskonsumenten in ein System bürokratischer Kontrolle integrierte und zudem Steuereinnahmen brachte. Dieser Cannabisdiskurs wurde in der Folge auch in Europa aufgegriffen. Auch hier wurde Marihuana als gefährliches Phantom profiliert, das mit dem ursprünglichen Hanf kaum mehr etwas gemeinsam hatte; alte Bauern wollten nicht glauben, dass es sich bei dem, was sie sich in ihrer Jugend arglos-neugierig in die Pfeife gestopft hatten, um denselben Stoff gehandelt habe. [17]
<35>
Anslinger ist auch der Erfinder der sogenannten Einstiegsdrogen-Theorie, nach der auf den Konsum von Cannabis zwangsläufig das Umsteigen auf noch stärkere Mittel, insbesondere Heroin, erfolgen soll. Im Sinne einer self-fulfilling prophecy ließ sich diese These in dem Maße bestätigen, in dem die Märkte für einzelne Stoffe durch ihre Illegalisierung auf Verbund geschaltet und damit durchlässiger werden konnten.
<36>
Weitere, die Betäubungsmittel betreffende Abkommen wurden in den Jahren 1936, 1948 und 1953 abgeschlossen. Nach 1945 wurde die UNO mit dieser ganzen Materie betraut. Eine herausragende Bedeutung kam der UNO-Single Convention on Narcotic Drugs von 1961 zu. Dieses Vertragswerk ersetzte die Internationale Opiumkonvention von 1912 und die darauf aufbauenden Zusatzabkommen und steckte den rechtlichen Rahmen auch für die heutige Drogendiskussion ab. Von den gesellschaftlichen Problemlagen her war dieses Einheitsabkommen allerdings rasch überholt. Der Kulturkampf um Drogen, der schon seit 1964 entbrannte, um dann ein wichtiger Aspekt der Rebellion der 1968er Bewegung zu werden, veränderte den Umgang mit psychoaktiven Stoffen fundamental und machte ihn zu einem wichtigen Element der Konfrontation zwischen Gegenkultur und Establishment.
<37>
Drogen wurden von der aufbegehrenden oder aussteigenden Jugend als Vehikel für Entspannung, neue Erfahrungen und psychedelische Trips verwendet. 1971 wurde das Einheitsabkommen auf psychotrope Substanzen wie LSD (das in den USA schon Mitte der 1960er Jahre verboten worden war) und Ecstasy erweitert. Bereits 1972 musste das Abkommen angesichts einer gefühlten „Drogenwelle“ und des Auftauchens von Designer-Drogen erneut verschärft werden. [18]
<38>
Diese Repressionspolitik schuf indessen einen goldenen Boden für das Geschäft auf dem Schwarzmarkt. Die Umsätze im Drogenhandel stiegen astronomisch an und die fehlende Regulierung im Finanzsektor führte zu immer dreisteren Verfahren der Geldwäscherei. Seit Mitte der 1980er Jahre richtete die UNO ihr Augenmerk denn auch stärker auf die Phänomene der organisierten Kriminalität und des illegalen Handels. Das sogenannte Wiener Abkommen von 1988 wollte rechtliche Instrumente, mit denen der Handel und die Finanzierung von Drogen weltweit bekämpft werden konnten, auf globaler Ebene harmonisieren und effizienter machen. Mit dieser Regulierung wurde allerdings gleichzeitig der Spielraum für Reformen weiter beschnitten. Im ausgehenden 20. Jahrhundert stellte die Ratifizierung dieses Abkommens, das 1990 in Kraft trat, einen Schwerpunkt der internationalen Drogenpolitik dar. Ein weiterer bestand in Versuchen, mit der Zerstörung von Anbauflächen und politischen Maßnahmen in Herstellerländern die Angebotsquellen versiegen zu lassen. Global betrachtet erwiesen sich beide Anstrengungen zur „Lösung des Drogenproblems“ trotz spektakulärer Teilerfolge schon mittelfristig als wirkungslos.
<39>
Repression ist eine Form sozialer Produktion. Das Verbotsregime, das auf Unterdrückung von Stoffen setzt und um dessen Legitimität und Praktikabilität bis heute gestritten wird, hat ein Drogenproblem mit spezifischen Konturen hervorgebracht, das vor allem in den 1980er und 1990er Jahren die mediale Berichterstattung in Atem hielt. [19] Im Verlauf des 20. Jahrhunderts und insbesondere seit den 1960er Jahren wurden die „Rauschgifte“, wie sie über die internationalen und nationalen Betäubungsmittelgesetze und weitere Abkommen definiert werden, zu den lukrativsten Handelsartikeln der Welt und die entsprechenden Märkte – vor allem für Heroin und Kokain, aber auch für Cannabis und eine steigende Zahl von sogenannter Designerdrogen – setzen Hunderte Milliarden Dollar um.
<40>
Akteure, die ihr Geschäftsgebaren weder an moralischen Grundsätzen noch an Rechtsnormen orientieren und sich um ethische und rechtliche Spielregeln menschlichen Zusammenlebens nicht weiter scheren, verspüren eine starke Neigung, sich in dieser florierenden Branche bemerkbar zu machen. Und wer darüber hinaus bereit ist, sich auf Risikokapital zu spezialisieren und hohe Verlustrisiken in Kauf zu nehmen, wird im Drogenhandel auch Erfolg haben – zumindest eine Zeit lang. Die in dieser Sparte entstandenen Unternehmen und Kartelle sind mit modernster Logistik ausgestattet. Sie verfügen über effiziente Gewaltabteilungen, die sie gegenüber den Wechselfällen der Politik wappnen und die es ihnen erleichtern, mit Rückschlägen umzugehen.
<41>
Sie wenden ein großes Repertoire von üblichen, unüblichen, unorthodoxen – man könnte auch sagen innovativen und kreativen – Geschäftsmethoden an und diversifizieren, transformieren und minimieren Risiken, so dass am Schluss die Kasse klingelt. Flugzeuge, U-Boote und Ballons gehören ebenso zum Transportarsenal wie die für die Beteiligten prekäre Beförderung von Drogen im Magen-Darmtrakt. Zur Abwicklung der Operationen stehen diesen Drogenhändlern auch heute internationale Finanzplätze zur Verfügung. Über „Waschmaschinen“ – jetzt gerade ist der Derivat- und der Kunsthandel stärker ins Gerede gekommen – wird Drogengeld gesäubert, anschließend in legale Kapitalkreisläufe eingespeist und dann in vergleichsweise sicheren Werten – in Immobilien, Aktienkapital, Rohstoffen, Wertpapieren aller Art – angelegt.
<42>
An beiden Enden der kriminellen Kapitalbildung mittels Drogengeschäften befinden sich zwei ökonomisch und sozial schwache Pole: die Produzenten der Drogenrohstoffe und die Konsumenten. Der Löwenanteil der verbotenen Drogen wird in Ländern angebaut, die wirtschaftlich wenig entwickelt sind und die sich mit einem failed state-Problem herumschlagen. In einigen zunehmend verarmten less developed countries – immer wieder in die Schlagzeilen geraten Afghanistan und Kolumbien, die Ländergruppe umfasst allerdings mehr als die Hälfte der Erdbevölkerung – stellt die Kultivierung der Ausgangspflanzen für verbotene Drogen, also Mohn, Koka und Hanf, eine Überlebensstrategie für breite, weithin mittellose Bevölkerungsschichten dar. Die Mühsal, der die ländliche Familienökonomie weithin ausgesetzt ist, wird verstärkt durch Rechtlosigkeit, Klientelwirtschaft und durch eine Weltwirtschaft, die nach dem Matthäus-Prinzip („Wer hat, dem wird gegeben“) funktioniert und privilegierte Positionen verstärkt.
<43>
Am Beispiel der Kokaproduktion wurde etwa gezeigt, wie die höchst gesundheitsschädigende Aufbereitung der Blätter einhergeht mit der Vernichtung großer Anbauflächen durch gefährliche Chemikalien, die mittels Flugzeugen und Helikoptern der Regierungen flächen deckend versprüht werden. [20] Solche Praktiken finden sich auch in Afghanistan, wo allerdings strategische Überlegungen und taktische Bündnisse auch die temporäre Toleranz des Opiumanbaus zur Folge haben können. Dies und die schwer bewaffnete Präsenz jener Agenturen der „organisierten Kriminalität“, die das Multimilliardengeschäft mit den Drogen kontrollieren, sorgten bisher dafür, dass Angriffe auf die Bauern als machtloses Bodenpersonal des hochfliegenden Geschäfts angebotsseitig wirkungslos blieben.
<44>
Am andern Ende der langen Verwertungskette liegen die Hauptabsatzgebiete in den urbanen Agglomerationen wirtschaftlich entwickelter Länder. Auch wenn die Konsumpraktiken sich längst globalisiert und auf ländliche Gebiete ausgeweitet haben, sind doch die lukrativen Umsatzpole für verbotene Stoffe da zu finden, wo sich die ungleich verteilte internationale Kaufkraft konzentriert. Dank der Verknappungstendenz, welche der Prohibitionspolitik inhärent ist, profitieren die entsprechenden Geschäftssegmente durch eine staatliche Hochpreisgarantie, die zwar durch aggressive Angebotsausweitungen immer wieder unterminiert wird, jedoch längerfristig intakt bleibt. So häufen sich die sozialen Probleme, die sich aus der brutalen Logik des Schwarzmarktes ergeben, bei den Konsumentinnen und Konsumenten an, die immer auch in den Kleinhandel involviert sind. Seit den 1980er Jahren haben sich in Metropolen von Konsumgesellschaften verschiedene Probleme verdichtet: Arbeitslosigkeit, Wohnungsnot, neue Armut. Parallel zum Abbau von Sozialversicherungssystemen nahm die soziale Ausgrenzungstendenz zu.
<45>
Dass in dieser Zeit die sogenannten „Drogenszenen“ entstanden, in denen Krankheit, Gewalt und Geld syndromartig amalgamierten, hing allerdings nicht direkt mit dem seit Mitte der 1980er Jahre ansteigenden sozialen Druck und auch nicht eindimensional mit der damals auftauchenden AIDS-Epidemie zusammen, sondern war primär das Resultat politischer Entscheidungen. Staat und Gesellschaft nahmen die sozialen Probleme zunehmend als politische Herausforderungen wahr. Das „Drogenproblem“ wurde zu einem kulturellen Code, über den eine politische Verständigung gesucht wurde. Den Drogenszenen und den Jugendlichen, die sie bevölkerten, kam ein hoher negativer Symbolwert zu. Diese marginalisierten Menschen gaben einprägsame Negativikonen der Massenmedien ab und standen als traurige Sinnbilder verunglückten Lebens im medialen Rampenlicht. Sie lieferten den Stoff für Elendsreportagen, die millionenfach über die Mattscheiben flimmerten. Drogen und das, was sie in diesem politischen Regime der Stigmatisierung bewirkten, erfüllten damit eine meist unausgesprochene gesellschaftliche Funktion, indem sie der moralischen Mehrheit in drastischer Weise zeigten, wohin es führt, wenn vom Pfad der Tugend abgewichen wird.
<46>
Komplementär zum raschen Reichwerden und glamourösen Erfolg, für den die Yuppies der 1980er Jahre standen, wurde das mörderische Beispiel des totalen Versagens im Drogenelend profiliert. Die offenen Drogenszenen können als mediale Konstrukte verstanden werden, welche die Normalität, die Konformität und die Leistungsbereitschaft stützten. Es kam ihnen (bezogen auf die Gesellschaft) eine integrative und (bezogen auf die Wirtschaft) eine produktivitätssteigernde Wirkung zu.
<47>
Dass die Dramatisierung des „Drogenproblems“ über die „offenen Szenen“ kontrafaktisch operierte, zeigen Schätzungen, die nachweisen, dass ein großer Teil der verbotenen „Betäubungsmittel“ – insbesondere Kokain, aber auch Hanf – als Leistungs- und Partydrogen fungieren. Sie werden nicht von sozial verwahrlosten Menschen am Rande der Gesellschaft, sondern von verhaltensunauffälligen, zum Teil sehr hart arbeitenden, pflichtbewussten und kaufkräftigen Erwerbstätigen konsumiert. Aus den genannten Gründen waren es allerdings die Drogenszenen, die als Verdichtungsräume für persönliche und soziale Probleme in den Brennpunkt der öffentlichen Aufmerksamkeit gerieten. Da diese Szenen per definitionem illegal sind, werden sie durch kriminelle Netzwerke beherrscht und von der anderen Seite durch die Polizei, welche die Kriminalität bekämpft, bedrängt. Die Versuche, die Versorgung der Schwarzmärkte mit den inkriminierten Stoffen auszutrocknen, haben in groteskem Ausmaß zu deren Überschwemmung mit immer neuen Angeboten geführt.
<48>
Repressionspolitik und Kriegslogik haben sich, wenn eine Jahrhundertbilanz gezogen wird, von niederschmetternder Wirkungslosigkeit und Kontraproduktivität erwiesen. Sie dienten der Politik zur Selbstinszenierung, sie schufen mächtige bürokratische Apparate, die ihre Legitimation aus einem Kampf gegen ein gesellschaftliches Übel bezogen und deren Arbeit nie einer Effizienz- und Qualitätskontrolle unterzogen wurde, so dass sie ihr offensichtliches Versagen in einen Beweis ihrer Unverzichtbarkeit umbiegen konnten. Dies nach der verqueren Logik: je größer das Problem, das aus einer repressiven Drogenprohibition resultierte, desto unverzichtbarer die Instanzen, welche diese Repression organisieren. Obwohl im vergangenen Jahrzehnt einige geistige Lockerungsübungen und eine gewisse Entideologisierung des „Drogenproblems“ zu erkennen sind, ist doch ein abrupter Systemwechsel nicht zu erwarten. [21]
<49>
Dennoch zeichnen sich Veränderungen ab. Auf internationaler Ebene wird man sich innerhalb der UNO immer stärker bewusst, dass der „Krieg gegen die Drogen“ angesichts eines prosperierenden Angebots illegaler Drogen an Boden verliert. Seit März 2009 wird im Rahmen einer weiteren Wiener Konferenz an einem neuen Konzept für den Kampf gegen den Drogenmissbrauch gearbeitet. Der bolivianische Präsident Evo Morales, der sich für eine Streichung der Koka-Blätter von der Liste verbotener Substanzen einsetzt, kaute während seiner Rede demonstrativ eben solche. Damit setzte er sich nicht nur für die Rechte der Koka-Bauern ein, sondern unterstrich auch symbolisch den Anspruch anderer Kontinente, ihre Sichtweise in einer während des ganzen 20. Jahrhunderts eurozentrischen und US-dominierten Diskussion zur Geltung zu bringen. [22]
<50>
Die Europäische Union spricht diese Problematik in ihrem zum selben Zeitpunkt veröffentlichten Bericht ebenfalls an. Der Bericht diagnostiziert eine Sackgasse der internationalen Drogenpolitik und stellt fest, trotz leichter Verbesserungen in einigen reichen Ländern habe sich die Lage in ärmeren Staaten massiv verschlechtert. Auf nationaler Ebene ist in vielen Ländern eine Drogenpolitik nach dem Suchtmodell „more of the same“ in Rechtfertigungsschwierigkeiten geraten und zum Auslaufmodell geworden. Der Fall der Schweiz, wo seit 1994 eine sogenannte „Viersäulenpolitik“, die neben Repression auch auf Prävention, Therapie und Schadensminderung setzt, zeigt, wie der Verelendung von Drogenabhängigen aus den „offenen Drogenszenen“ erfolgreich entgegengewirkt werden kann. [23]
<51>
Die aufschlussreichsten und dynamischsten Prozesse spielen sich heute ganz allgemein in der pragmatischen Reorientierung der Drogenpolitik ab. Hier werden Ansätze einer Substitutionstherapie im Zeichen von harm reduction erprobt. [24] Grundlegend ist dafür die Einsicht, dass das Drogenproblem weder eine zu lösende noch eine lösbare Aufgabe ist. Diesbezüglich muss der Staat – in einem liberalen Sinne – proaktiv und selbstbewusst resignieren. Er hat nämlich gar kein Recht, Menschen zu ihrem Glück zu zwingen. Noch weniger ist er befugt, sie aus lauter gutem Willen ins Unglück zu stürzen. Über Jahrzehnte hinweg wurden mit dem ideologisch aufgerüsteten Schlachtruf einer „Lösung des Drogenproblems“ drogenabhängige Menschen dem Schwarzmarkt und damit der Rechtlosigkeit ausgeliefert und in Konsumpraktiken hineingezwungen, die eine hohe Ansteckungsgefahr aufweisen und die für eine große Zahl mit Krankheit und Tod endeten. Zugleich stärkt die Drogenprohibition in vielen, vor allem in verarmten Ländern Kräfte, die auf die Zerstörung der Staatlichkeit hinarbeiten. Der obsessive Ordnungswille in reichen Ländern und die Destruktion rechtsstaatlicher Ordnung in armen Ländern geraten so in eine desaströse und asymmetrische Wechselwirkung, die das Nord-Süd-Gefälle verstärkt.
<52>
Solche Vorgänge werden heute besser verstanden als noch vor einiger Zeit, als sie fast vollständig hinter der moralischen Nebelwand einer „drogenfreien Welt“ verschwanden. Obwohl dieser Slogan von jenen, die es nicht lassen können, hochgehalten wird und auch innerhalb der UNO immer wieder ertönt, könnte der Beginn des 21. Jahrhunderts dennoch den Übergang in eine neue Phase der Post-Prohibition markieren, in der sich die Drogenproblematik einerseits sozial diversifiziert und differenziert und andererseits entdramatisiert. Die Abkehr von einer einfältigen, manichäischen Problemstrukturierung könnte in einer positiven Feedbackschlaufe Drogen enttabuisieren, normalisieren und in die Konsumgesellschaft integrieren.
<53>
Dies wiederum würde zweifellos politische Folgen haben. Die willkürliche Unterscheidung von legalen und illegalen Drogen würde einbrechen. Die medizinisch fassbaren Probleme, die auf Drogengebrauch zurückgehen, würden ebenso selbstverständlich in eine ärztliche Behandlungspraxis integriert wie jene, die mit Bergsteigen, Badeferien und Übergewicht zusammenhängen. Gleichzeitig würden die stark aufstrebenden Präventionsbemühungen, die in verschiedensten Bereichen der Gesellschaft festzustellen sind und sich längst nicht mehr auf die Unterdrückung gesundheitsschädlicher Praktiken beschränken, sondern auf ein Enhancement, das heißt eine präventionsmedizinische Steigerung der Lebensmöglichkeiten, abzielen, das Drogenproblem neu formatieren. [25] Polizeiliche Repression würde weithin in sozialen Anpassungsdruck transformiert, wie das heute beim Tabakrauchen festzustellen ist. Damit werden Problemlagen erkennbar, die deutlich machen, dass die Abkehr von der Drogenprohibition nicht in einen ursprünglichen „freien Zustand“ zurückführt.
<54>
Die angedeutete Entwicklung birgt allerdings mehr Potenziale für einen selbstbestimmten Umgang mit Drogen als eine Politik, welche Drogenkonsumenten zu Sündenböcken erklärt und sie exemplarisch abstraft. Wer dies als Verlust an Lebensspannung wertet und an außerordentlichen Existenzentwürfen festhalten möchte, wer den Willen zu transzendentalem Erleben nicht aufgibt und weiterhin durch den Hunger nach Ergriffenheit getrieben wird, wer zudem den faszinierenden Drogenschreckgespenstern nachtrauert, die im 19. Jahrhundert die Poeten der Bohème und die Polizisten vom Dienst gleichermaßen beschworen haben, dem bleibt frei gestellt, sich mit Erfahrungsdrogen durch die „Pforten der Wahrnehmung“ aus der postheroischen Gesellschaft der Gegenwart in ungeahnte psychedelische Welten katapultieren zu lassen. Diese Freiheit konnte auch das Prohibitionsregime des 20. Jahrhunderts nie zunichte machen.
Prof. Dr. Jakob Tanner
Universität Zürich
Historisches Seminar
Forschungsstelle für Sozial- und Wirtschaftsgeschichte
Rämistrasse 64
CH – 8001 Zürich
jtanner@hist.uzh.ch
[1] Für einen Überblick vgl. Richard P. Davenport-Hines: The Pursuit of Oblivion. A Global History of Narcotics, New York 2002. Grundlegend sind auch: Thomas Hengartner / Christoph Maria Merki (Hg.): Genussmittel. Ein kulturgeschichtliches Handbuch, Frankfurt a.M. 1999; Sebastian Scheerer / Irmgard Vogt (Hg.): Drogen und Drogenpolitik. Ein Handbuch, Frankfurt a.M. / New York 1989; Gisela Völger unter Mitarbeit von Karin von Welck und Aldo Legnaro (Hg.): Rausch und Realität. Drogen im Kulturvergleich, 3 Bde, Köln 1985; Wolfgang Schivelbusch: Das Paradies, der Geschmack und die Vernunft. Eine Geschichte der Genussmittel, München / Wien 1980; zur aktuellen Entwicklung vgl. Günter Amendt: No drugs no future: Drogen im Zeitalter der Globalisierung, Hamburg / Wien 2003.
[2] Peter von Matt: Die tintenblauen Eidgenossen. Über die literarische und politische Schweiz, München / Wien 2001, 9-11. Der Autor hält diese Aussagen für transnational generalisierungsfähig.
[3] Jacques Derrida: Rhétorique de la drogue, in: L’esprit des drogues. Autrement. Série mutations. No. 106, April 1989, 197-214.
[4] Gregory Austin: Die europäische Drogenkrise des 16. und 17. Jahrhunderts, in: Gisela Völger u.a. (Hg.): Rausch und Realität, I, 1982, 115–133; Annerose Menninger: Genuss im kulturellen Wandel: Tabak, Kaffee, Tee und Schokolade in Europa (16.-19. Jahrhundert), 2. Aufl., Stuttgart 2008.
[5] Vgl. dazu unter anderen Arthur Waley: The Opium War Through Chinese Eyes, London 1958; Chang Hsin-Pao: Commissioner Lin and the Opium War, Cambridge 1964; Peter W. Fay: The Opium War, 1840-1842: Barbarians in the Celestial Empire in the Early Part of the Nineteenth Century and the War by Which They Forced Her Gates Ajar, Chapel Hill 1975; Chung Tan: China and the Brave New World: a Study of the Origins of the Opium War 1840-42, Durham, N.C. 1978; Keith McMahon: The Fall of the God of Money: Opium Smoking in Nineteenth-Century China, Lanham / Oxford 2002.
[6] Paul C. Winther: Anglo-European Science and the Rhetoric of Empire: Malaria, Opium, and British Rule in India, 1756-1895, Lanham 2003; David Anthony Bello: Opium and the Limits of Empire: Drug Prohibition in the Chinese interior, 1729-1850, Cambridge 2005; Yangwen Zheng: The Social Life of Opium in China, Cambridge 2005.
[7] Vgl. Alain Ehrenberg / Patrick Miignon (Hg.): Drogues, politique et société, Paris 1992; David T. Courtwright: Forces of Habit: Drugs and the Making of the Modern World, 3. Aufl., Cambridge 2001; Geoffrey Harding: Opiate Addiction, Morality and Medicine. From Moral Illness to Pathological Disease, New York 1988.
[8] Die Darstellung der beiden folgenden Abschnitte folgt stark der Publikation: Renée Renggli / Jakob Tanner: Das Drogenproblem. Geschichte, Erfahrungen, Therapiekonzepte, Berlin / Heidelberg / New York 1994, 92ff.
[9] Elmer C. Sandmeyer: The Anti-Chinese Movement in California, Urbana 1939; Roger Daniels: Asian America. Chinese and Japanese in the United States since 1850, Seattle / London 1988.
[10] Albert Wissler: Die Opiumfrage. Eine Studie zur weltwirtschaftlichen und weltpolitischen Lage der Gegenwart, Jena 1931, 154f.
[11] Zu diesem Aspekt, der auch für die Schweiz von Bedeutung war, vgl. Jakob Tanner: Rauschgiftgefahr und Revolutionstrauma. Drogenkonsum und Betäubungsmittelgesetzgebung in der Schweiz der 1920er Jahre, in: Sebastian Brändli u.a. (Hg.): Schweiz im Wandel. Studien zur neueren Gesellschaftsgeschichte, Basel 1990, 397-416.
[12] Charles E. Terry / Pellens Mildred: The Opium Problem, New York 1928.
[13] David T. Courtwright: Dark Paradise. Opiate Addiction in America before 1940, Cambridge, Massachusetts. 1982. Vgl. auch ders.: Addicts who survived. An oral history of narcotic use in America, 1923-1965, Knoxville, Tennessee 1989.
[14] Vgl. Louise Elisabeth Eisenlohr: International Narcotic Control, London / Wokin, 1934; Peter Lowes: The Genesis of International Narcotic Control, Genf 1966; Arnold H. Taylor: American Diplomacy and the Narcotic Traffic, 1900-1939: A Study in International Humanitarian Reform, Durham N.C. 1969; David F. Musto: The American Disease: Origins of Narcotic Control, New Haven 1973. Kritischer sind: Arnold S. Trebach / Kevin B. Zeese (Hg.): Drug Prohibition and the Conscience of Nations, Washington 1990. Einen alternativen Ansatz am Beispiel der Alkoholprohibition entwickelt Joseph R. Gusfield: Symbolic Crusade: Status Politics and the American Temperence Movement, Urbana 1963. Auf dieser Argumentationslinie siehe auch: Michael Woodiwiss: Crime, Crusades and Corruption: Prohibitions in the United States 1900-1987, London 1988.
[15] Zur Geschichte der Hanfprohibition vgl. Jack Herer: Die Wiederentdeckung der Nutzpflanze Hanf, Cannabis Marihuana, Frankfurt a.M. 1997 (mit einer Kurzstudie vom Katalyse-Institut für angewandte Umweltforschung e.V, hg. von Mathias Bröckers); Hans-Georg Behr: Von Hanf ist die Rede: Kultur und Politik einer Droge, Frankfurt a.M. 2000.
[16] Vgl. dazu etwa Rudolf Gelpke: Vom Rausch im Orient und Okzident, Stuttgart 1966.
[17] Auf die lange Tradition von Hanf als Heilmittel weist hin: Christian Rätsch: Hanf als Heilmittel. Eine ethnomedizinische Bestandsaufnahme, Solothurn / Wien 1992.
[18] Über diese rechtlichen Aspekte informiert (bis Ende der 1980er Jahre) Francis Caballero: Droit de la drogue, Paris 1989.
[19] Vgl. unter anderen Pino Arlacchi: Mafiose Ethik und der Geist des Kapitalismus. Die unternehmerische Mafia, Frankfurt a.M. 1989; Observatoire géopolitique des drogues (OGD): Der Welt-Drogen-Bericht: ein Jahresbericht, München 1993; Alain Labrousse / Alain Wallon (Hg.): Der Planet der Drogen. Analyse einer kriminellen Weltmacht, Frankfurt a.M. 1996; Loretta Napoleoni: Die Zuhälter der Globalisierung: über Oligarchen, Hedge Fonds, ’Ndrangheta’, Drogenkartelle und andere parasitäre Systeme, München 2008; aus globalpolitischer Perspektive: Surya Narayan Yadav: Terrorism, Drug-Trafficking and Organised Crime: Challenges for International Peace and Security, New Delhi 2009. Konsumenten und Kleinhändler behandelt Bernd Werse (Hg.): Drogenmärkte: Strukturen und Szenen des Kleinhandels, Frankfurt a.M. / New York 2008.
[20] Zorka Domic: L’Etat Cocaïne. Science et politique de la feuille à la poudre, Paris 1992.
[21] Vgl. die kritische und zugleich ernüchternde Analyse von Andreas Bummel: Eine Ideologie am Ende: Die globale Drogenprohibition (26.06.2004) http://www.heise.de/tp/r4/artikel/17/17708/1.html <8.11.2009>.
[22] Aufschlussreiche Informationen dazu bietet Manfred Kappeler: Drogen und Kolonialismus. Zur Ideologiegeschichte des Drogenkonsums, Frankfurt a.M. 1991.
[23] Für die neuere Entwicklung und die Perspektiven in der Schweiz vgl. Bundesamt für Gesundheit (Hg.): Die Drogenpolitik der Schweiz (MaPaDro III). Drittes Maßnahmenpaket des Bundes zur Verminderung der Drogenprobleme (MaPaDro III) 2006-2011 http://www.bag.admin.ch/shop/00035/00204/index.html?lang=de <8.11.2009>.
[24] Schon früh für eine pragmatische Orientierung der Drogenpolitik plädierte Stephan Quensel: Drogenelend. Cannabis, Heroin, Methadon: für eine neue Drogenpolitik, Frankfurt a.M. 1982; vgl. auch ders.: Mit Drogen leben – Erlaubtes und Verbotenes, Frankfurt a.M. 1985. Zur aktuellen Diskussion um die Substitutionspolitik vgl. Jakob Tanner: Drogen, Abhängigkeit und Substitution: historischer Rückblick und Überlegungen zur aktuellen Situation, in: Abhängigkeiten, 2007, 6-21.
[25] Sheila M. Rothman / David J. Rothman: The Pursuit of Perfection. The Promise and Perils of Medical Enhancement, New York 2003; Linda F. Hogle: Enhancement Technologies and the Body, in: Annual review of anthropology 34 (2005), 695-716.
LAAM, or levo-alpha-acetyl-methadol, is a synthetic opioid used in the treatment of opioid addiction. Approved in 1993 by the U.S. Food and Drug Administration, LAAM is considered to be similar to methadone in its effects, which include analgesia, sedation and respiratory depression. LAAM is indicated for use in the treatment and maintenance of opioid dependence, most often when patients don’t benefit from other replacement therapies such as methadone and buprenorphine. Because of its long-acting formula, LAAM is taken 2-3 times per week, whereas methadone is a daily treatment. Doses are administered in approved medical facilities and take-home doses are prohibited under federal regulations. It works by creating a cross-tolerance to other opiates, blocking the euphoric effects and controlling drug cravings.
Narcotic maintenance therapy, or substitution therapy, came about in the late 1960s to early 1970s in response to escalating use of heroin. Interest in expanding available programs was heightened when cases of HIV, AIDS, tuberculosis and hepatitis skyrocketed among intravenous drug users who shared needles. Many experts believe that providing maintenance therapies will help to curb problems associated with drug use, including crime, disease, unemployment, child neglect and homelessness.
LAAM can be highly addictive and is considered a Schedule II controlled substance in the U.S. The federal Drug Enforcement Agency classifies drugs based on their potential to be habit-forming and to lead to abuse. Tolerance and dependence can set in quickly with repeated use. This makes LAAM susceptible to illicit use and diversion. It is dangerous – potentially fatal- to mix LAAM with drugs like benzodiazepines, alcohol, sleeping pills, antidepressants or other opiates. Mixing pills can lead to sedation, drowsiness, unconsciousness and death. Side effects when used as prescribed could include body aches, flu-like symptoms, hot flashes, abdominal pain, constipation, dry mouth, diarrhea, vomiting, nausea, abnormal dreams, anxiety, depression, headaches, insomnia, rash, sweating and blurred vision.
Opiate addiction is a chronic problem with a high rate of relapse. Using an opiate to treat an opiate addiction may work for some, but is not effective for everyone. Detoxing from narcotics can cause extreme anxiety and severe withdrawal symptoms if not approached properly. Withdrawal symptoms associated with opiate addiction include cramps, spasms, diarrhea, yawning, vomiting, flu-like symptoms, cold sweats, aches, agitation, anxiety, insomnia and nightmares. Medically-supervised detox programs are often recommended to help wean users from dangerous opiates. Rapid detox programs have also been gaining ground in recent years, treating opiate addiction quickly, while eliminating the painful withdrawal phase.
Opiate drugs are used to help people reduce their dependence on heroin (an opiate drug). Methadone needs daily doses, but the effects do not last 24 hours for many people. A dose of LAAM (levomethadyl acetate hydrochloride) works for two or three days. LAAM is not as widely available internationally as methadone, and may be withdrawn from the market because of concerns about life-threatening effects on the heart. The review found that LAAM is more effective than methadone at reducing heroin dependence, but there was not enough evidence from trials to draw conclusions about safety.
LAAM
The National institute of Drug Abuse is currently testing LAAM, levo-alpha-acetylmethadol-hydrochloride, a synthetic new opiate substitute, for use in heroin-addiction treatment.
LAAM is a white, crystalline, soluble, morphine-Tike compound, a central-nervous-system depressant being investigated , as a longer-lasting alternative to methadone currently the most widespread treatment for addiction. The drug is as highly addictive as methadone, but experts are generally in agreement that opiate addiction-can be stemmed only by the substitution of: another addiction.
At present, a reformed junkie undergoing treatment must report to a methadone clinic once a day to receive his „medicine,“ while a LAAM patient’s dose can last up to seventy-two hours. This time factor is he big advantage of` LAAM. The drug produces a cross-tolerance to other- opiates: Shooting up while taking LRAM will .be a waste of the addict’s time and money, since ll of heroin’s euphoric effect will be blocked. As it is taken‘ orally, LAAM eliminate& the dangerous side effects of needle use. Another important factor is that the drug: suppresses the users uncontrollable desire: for heroin and other. opiates both during he time he is addicted and after he has been detoxified. LRAM takes effect about two to six hours after ingestion, blocking potential withdrawal symptoms. In about two weeks the patient is effectively weaned from heroin to LAAM, without discomfort.
Scientists believe infrequent cases of LAAM overdose may actually be due to multi-drug use. Alcohol and LAAM are like oil and water, not to be mixed under. any circumstances. People with low narcotics tolerance are also potential LAAM overdose cases. No illicit street sale of the drug has yet been reported. Indeed, there may never be a thriving black market in LAAM, even if it does become widely dispensed, since it lacks the one. ingredient the drug user seeks-it won’t get him high. The drug’s sustained, level effect makes the addict simply feel „normal.“ Patients do not feel sedated or euphoric, and preliminary findings :indicate they seem to be more alert than those taking methadone.
Since the addict has to visit his drug clinic for LAAM only three times a week, psychological dependency on daily heroin or methadone use is reduced, allowing for alteration of previously established negative drug behavior patterns: He begins to feel like a member‘ of the drug-free world, although present indications are that he will have to be maintained on LAAM indefinitely. He does not have to take the drug home on weekends, since the effect of a dose lasts from Friday to Monday. This factor may minimize potential abuse and diversion of LAAM to the illicit market.
Side effects vary from person to person. Mild sweating, constipation, anxiety, insomnia, and nausea have been reported sporadically. Since LAAM’s effect on pregnancy and childbearing is unknown, all six thousand test subjects thus far have been male.
If LAAM’s viability as a long-lasting, effective narcotic alternative‘ is ultimately proved, treatment of addiction may become more economical and efficient. Three times the number of addicts could be treated in existing drug centers at one third the expense of methadone therapy.
LAAM’s main advantage over heroin is its legal, although restricted, status. LAAM’s primary advantage over methadone is the necessity for less frequent administration. The junkie can trade the expensive and socially disruptive monkey on his back for the apparently safe, convenient, and free drug LAAM.
Orlaam
(levomethadyl acetate hydrochloride)
Due to its potential for serious and possibly life-threatening, proarrhythmic effects, LAAM should be reserved for use in the treatment of opiate-addicted patients who fail to show an acceptable response to other adequate treatments for opiate addiction, either because of insufficient effectiveness or the inability to achieve effective dose due to intolerable adverse effects from those drugs (see WARNINGS and Contraindications ).
Cases of QT prolongation and serious arrhythmia (torsade de pointes) have been observed during post-marketing treatment with ORLAAM. Based on these reports, all patients should undergo a 12-lead ECG prior to administration of ORLAAM to determine if a prolonged QT interval (QTc greater than 430 [male] or 450 [female] ms) is present. If there is a prolonged QT interval, ORLAAM should NOT be administered. For patients in whom the potential benefit of ORLAAM treatment is felt to outweigh the risks of potentially serious arrhythmias, an ECG should be performed prior to treatment, 12-14 days after initiating treatment, and periodically thereafter, to rule out any alterations in the QT interval.
ORLAAM should be administered with extreme caution to patients who may be at risk for development of prolonged QT syndrome (e.g., congestive heart failure, bradycardia, use of a diurectic, cardiac hypertrophy, hypokalemia, or hypomagnesemia).
ORLAAM is metabolized to active metabolites by the cytochrome P450 isoform, CYP3A4. Therefore, the addition of drugs that induce this enzyme (such as rifampin, phenobarbital, and phenytoin) or inhibit this enzyme (such as ketoconazole, erythromycin, and saquinavir) could increase the levels of parent drug or its active metabolites in a patient that was previously at steady-state, and this could potentially precipitate serious arrhythmias, including torsade de pointes (see PRECAUTIONS , Drug Interactions ).
CONDITIONS FOR DISTRIBUTION AND USE OF ORLAAM (42 CFR Part 8)
ORLAAM, used for the treatment of opiate addiction, shall be dispensed only by Opioid Treatment Programs (OTPs) certified by SAMHSA under 42 CFR Part 8, and registered by the Drug Enforcement Administration under 21. U.S.C. 823(g)(1). This does not preclude the maintenance or detoxification treatment of a patient who is hospitalized for medical conditions other than opiate addiction and who requires temporary maintenance for concurrent opiate addiction during the critical period of the patients hospitalization. Failure to abide by these requirements may result in injunction precluding operation of the program, revocation of the program approval, and possible criminal prosecution.
ORLAAM has no recommended uses outside of the treatment of opiate addiction.
ORLAAM (brand of levomethadyl acetate hydrochloride) is a synthetic opiate agonist. Chemically, it is levo-alpha-6- dimethylamino-4, 4-diphenyl-3-heptyl acetate hydrochloride, C 23 H 31 NO 2 · HCl. It is also known as levo-alpha-acetyl-methadol hydrochloride (LAAM).
The compound is a white crystalline powder, soluble in water (>15 mg/mL), ethanol, and methyl ethyl ketone. The octanol:water partition coefficient of LAAM is 405:1 at physiologic pH. Doses of ORLAAM (LAAM) are always expressed as the weight of the hydrochloride salt (molecular weight 389.95).
ORLAAM is an aqueous solution which is diluted for oral administration. Each one mL of ORLAAM contains: Levomethadyl acetate hydrochloride (LAAM) 10 mg. Inactive ingredients: Methylparaben, propylparaben, hydrochloric acid and water.
Last reviewed on RxList: 12/8/2004
ORLAAM is indicated for the management of opiate dependence. ORLAAM should be reserved for the use in treatment of opiate-addicted patients who fail to show an acceptable response to other adequate treatments for opiate addiction, either because of insufficient effectiveness or the inability to achieve effective dose due to intolerable adverse effects from those drugs (see Black Box Warning ).
ORLAAM produces opioid effects and a high degree of opioid tolerance that inhibits drug-seeking behavior and blocks the euphoria produced by the usual doses of heroin. The dose of ORLAAM in each patient should be adjusted to achieve the optimal therapeutic benefit with acceptable adverse opioid effects (see INDIVIDUALIZATION OF DOSAGE ).
ORLAAM must always be diluted before administration, and should be mixed with diluent prior to dispensing. To avoid confusion between prepared doses of ORLAAM and methadone, the liquid used to dilute ORLAAM should be a different color from that used to dilute methadone in any specific clinic setting.
ORLAAM is usually administered three times a week, either on Monday, Wednesday and Friday, or on Tuesday, Thursday and Saturday. If withdrawal is a problem during the 72-hour inter-dose interval, the preceding dose may be increased. In some cases, an every-other-day schedule may be appropriate (see INDIVIDUALIZATION OF DOSAGE ).
The usual doses of ORLAAM must not be given on consecutive days because of the risk of fatal overdose. No dose mentioned in this label is ever meant to be given as a daily dose (see WARNINGS ).
The initial dose of ORLAAM for street addicts should be 20 to 40 mg. Each subsequent dose, administered at 48- or 72-hour intervals, may be adjusted in increments of 5 to 10 mg until a pharmacokinetic and pharmacodynamic steady-state is reached, usually within 1 or 2 weeks (see INDIVIDUALIZATION OF DOSAGE ).
Patients dependent on methadone may require higher initial doses of ORLAAM. The suggested initial 3-times-a-week dose of ORLAAM for such patients is 1.2 to 1.3 times the daily methadone maintenance dose being replaced. This initial dose should not exceed 120 mg and subsequent doses, administered at 48- or 72-hour intervals, should be adjusted according to clinical response.
Most patients can tolerate the 72-hour inter-dose interval during the induction period. Some patients may require additional intervention (see INDIVIDUALIZATION OF DOSAGE ). If additional opioids are required, and the patient is not eligible or appropriate for take home doses of ORLAAM, supplemental methadone in small doses should be given rather than giving ORLAAM on two consecutive days. Take-home doses of ORLAAM and methadone always pose a risk in this setting and physicians should carefully weigh the potential therapeutic benefit against the risk of diversion.
In some cases, where the degree of tolerance is unknown, patients can be started on methadone to facilitate more rapid titration to an effective dose, then converted to ORLAAM after a few weeks of methadone therapy.
The crossover from methadone to ORLAAM should be accomplished in a single dose; complete transfer to ORLAAM is simpler and preferable to more complex regimens involving escalating doses of ORLAAM and decreasing doses of methadone.
Dosage should be carefully titrated to the individual; induction too rapid for the patient’s level of tolerance may result in overdose. Serious hazards, as seen in association with all narcotic analgesics, are respiratory depression and, to a lesser extent, circulatory depression.
Most patients will be stabilized on doses in the range of 60 to 90 mg, 3-times-a-week. Doses as low as 10 mg and as high as 140 mg three times a week have been given in clinical studies.
Supplemental dosing over the 72-hour inter-dose interval (weekend) is rarely needed. For example, if a patient on a Mon./Wed./Fri. schedule complains of withdrawal on Sundays, the recommended dosage adjustment is to increase the Friday dose in 5 to 10 mg increments up to 40% over the Mon./Wed. dose or to a maximum of 140 mg.
Most patients do not experience withdrawal during the 72-hour inter-dose interval after reaching pharmacological steady-state with or without adjustment of the Friday dose. If additional opioids are required, and the patient is not eligible or appropriate for take home doses of ORLAAM, small doses of supplemental methadone should be given rather than giving ORLAAM on two consecutive days. Take-home doses of ORLAAM and methadone always pose a risk in this setting and physicians should carefully weigh the potential therapeutic benefit against the risk of diversion (see
If withdrawal symptoms persist after adjustment of dose, consideration may be given to every-other-day dosing if clinic hours permit. If the clinic is not open seven days a week and every-other day dosing is not practical, the patient’s schedule may be adjusted so the 72-hour interval occurs during the week and the patient can come to the clinic to receive a supplemental dose of methadone (see INDIVIDUALIZATION OF DOSAGE ).
The maximum total amount of ORLAAM recommended for any patient is 140-140-140 mg or 130-130-180 mg on a thrice-weekly schedule or 140 mg every other day.
If it is determined that a patient is responsible in handling opioid drugs then ORLAAM take-home doses are permitted. Refer to 42 CFR Part 8 for specific restrictions.
Following a lapse of one ORLAAM dose:
Following a lapse of more than one ORLAAM dose:
Patients should be reinducted at an initial dose of 1/2 or 3/4 their previous ORLAAM dose, followed by increases of 5 to 10 mg every dosing day (48- or 72-hours intervals) until their previous maintenance dose is achieved. Patients who have been off of ORLAAM treatment for more than a week should be reinducted.
Patients maintained on ORLAAM may be transferred directly to methadone. Because of the difference between the two compounds‘ metabolites and their pharmacological half-lives, it is recommended that methadone be started on a daily dose at 80% of the ORLAAM dose being replaced; the initial methadone dose must be given no sooner than 48 hours after the last ORLAAM dose. Subsequent increases or decreases of 5 to 10 mg in the daily methadone dose may be given to control symptoms of withdrawal or, less likely, symptoms of excessive sedation, in accordance with clinical observations.
There is a limited experience with detoxifying patients from ORLAAM in a systematic manner, and both gradual reduction (5 to 10% a week) and abrupt withdrawal schedules have been used successfully. The decision to discontinue ORLAAM therapy should be made as part of a comprehensive treatment plan (see INDIVIDUALIZATION OF DOSAGE ).
ORLAAM is a solution of a potent narcotic (LAAM). There are no known specific hazards associated with dermal and aerosol exposure to ORLAAM. In case of accidental dermal exposure, promptly remove contaminated clothing and rinse the affected skin with cool water.
Sales of ORLAAM are restricted to clinics that have received training in its use. Since ORLAAM can be potentially dangerous if diverted, appropriate security measures should be taken to safeguard stock of ORLAAM as required by 21 CFR 1301.74.
Physicians should be alert to palpitations, syncope, or other symptoms suggestive of episodes of irregular cardiac rhythm in patients taking ORLAAM and promptly evaluate such cases (see WARNINGS , Effects on Cardiac Conduction ).
Patients presenting for ORLAAM treatment are frequently in withdrawal from heroin or other opiates. They may display typical withdrawal symptoms which should be differentiated from ORLAAM’s side effects. Patients may exhibit some or all of the following signs and symptoms associated with withdrawal from opiates: lacrimation, rhinorrhea, sneezing, yawning, perspiration, gooseflesh, fever, chilliness alternating with flushing, restlessness, irritability, insomnia, weakness, anxiety, depression, dilated pupils, tremors, tachycardia, abdominal cramps, body aches, anorexia, nausea, vomiting, diarrhea, and weight loss. Control of such symptoms is a primary goal of therapy. However, because of the slow onset and long half-lives of ORLAAM, nor-LAAM and dinor-LAAM, overly aggressive increases in dosage to control these withdrawal symptoms with ORLAAM may result in overdose (see INDIVIDUALIZATION OF DOSAGE ).
The interaction between the development and maintenance of opioid tolerance and ORLAAM dose can be complex. Dose reduction is recommended in cases where patients develop signs and symptoms of excessive ORLAAM effect, characterized by complaints of „feeling wired“, poor concentration, drowsiness, and possibly dizziness on standing.
Patients may experience withdrawal symptoms (nasal congestion, abdominal symptoms, diarrhea, muscle aches, anxiety) over the 72-hour dosing interval if the dose of ORLAAM is too low. This may be managed as described under INDIVIDUALIZATION OF DOSAGE , but physicians should be alert to the possible need for dose or dose schedule adjustments if patients complain of weekend withdrawal symptoms in the last day of the 72-hour dosing interval.
The following adverse events were observed in the 25-site, 623-patient usage study in male and female opiate addicts (see CLINICAL TRIALS ). These signs and symptoms were reported during the second and third months of treatment with ORLAAM, and were considered severe enough to require medical evaluation. In this study, both questionnaires and spontaneous reports were used to gather information. Questionnaire-elicited symptom frequencies were about five times as frequent as the spontaneous reporting frequencies given below.
Body as a Whole Asthenia * , back pain, chills, edema, hot flashes (males 2:1), flu syndrome and malaise (11%).
Gastrointestinal Abdominal pain * , constipation * , diarrhea, dry mouth, nausea and vomiting.
Musculoskeletal Arthralgia *
Nervous System Abnormal dreams, anxiety, decreased sex drive, depression, euphoria, headache, hypesthesia, insomnia (9.1%), nervousness * , somnolence.
Respiratory Cough, rhinitis, and yawning.
Skin/appendages Rash, sweating * .
Special Senses Blurred vision.
Urogenital Difficult ejaculation * , impotence * .
*Reactions in 3-9% of patients; reactions in 1-3% are unmarked.
Cardiovascular Postural hypotension.
Musculoskeletal Myalgia.
Special Senses Tearing.
These reactions were reported with low frequency in controlled and uncontrolled studies of LAAM, are not known to be causally related to the administration of the drug, and are provided as alerting information for physicians.
Cardiovascular Hypertension
Hepatic Hepatitis and abnormal liver function tests.
Urogenital Amenorrhea, pyuria.
The following adverse reactions have been reported in the post-marketing setting (all reactions in less than 1% of patients).
Body as a Whole Altered hormone level, chest pain.
Cardiovascular QT interval prolongation, torsade de pointes, cardiac arrest, ST segment elevation, ventricular tachycardia, myocardial infarction, angina pectoris, syncope, migraine.
Nervous System Convulsions, confusion, hallucination, incoordination, amnesia.
Urogenital Breast enlargement.
ORLAAM is a Schedule II controlled substance under the Federal Controlled Substances Act. ORLAAM produces dependence of the morphine-type and has potential for abuse. Tolerance and physical dependence will develop upon repeated administration. As with methadone and any other narcotic administered to narcotic addicts, ORLAAM is at risk for diversion and illicit use, and should be handled accordingly (see WARNINGS ).
No interaction studies have been performed in humans. ORLAAM is metabolized by the cytochrome P450 isoform, CYP3A4. The addition of drugs that induce this enzyme could increase the levels of active metabolites in a patient that was previously at steady-state.
Potentially Arrhythmogenic Agents Any drug known to have the potential to prolong the QT interval should not be used together with ORLAAM. Possible pharmacodynamic interactions can occur between ORLAAM and potentially arrhythmogenic agents such as class I or III antiarrhythmics, antihistamines that prolong the QT interval, antimalarials, calcium channel blockers, neuroleptics that prolong the QT interval, and antidepressants
Caution should be used when prescribing concomitant drugs known to induce hypokalemia or hypomagnesemia as they may precipitate QT prolongation and interact with ORLAAM. These would include diuretics, laxatives and supraphysiological use of steroid hormones with mineralocorticoid potential.
Polydrug and Alcohol Abusers Patients who are known to abuse sedatives, tranquilizers, propoxyphene, antidepres-sants, benzodiazepines, and alcohol should be warned of the risk of serious overdose if these substances are taken while on ORLAAM maintenance.
Interaction with Narcotic Antagonists, Mixed Agonists/Antago-nists, Partial Agonists, and Pure Agonists As with other mu agonists, patients maintained on ORLAAM may experience withdrawal symptoms when administered pure narcotic antagonists, such as naloxone, naltrexone, and nalmefene, or when administered mixed agonists/antagonists or partial agonists such as pentazocine, nalbuphine, butorphanol, and buprenorphine.
In addition, agonists such as meperidine and propoxyphene, which are N-demethylated to long-acting, excitatory metabolites, should not be used by patients taking ORLAAM because they would be ineffective unless given in such high doses that the risk of toxic effects of the metabolites becomes unacceptable.
Anesthesia and Analgesia Patients receiving ORLAAM will develop a similar level of tolerance for opioids as patients receiving methadone. Anesthetists and other practitioners should be prepared to adjust their management of these patients accordingly.
Other Drug Interactions The anti-tuberculosis drug rifampin has been found to produce a marked (50%) reduction in serum methadone levels, leading to the appearance of symptoms of withdrawal in well-stabilized methadone maintenance patients. Similar effects on serum methadone levels have been observed for carbamazepine, phenobarbital, and phenytoin. The presumed mechanism for this effect is the induction of methadone metabolizing enzymes. Since ORLAAM is metabolized into a more active metabolite, nor-LAAM, administration of these drugs may increase ORLAAM’s peak activity and/or shorten its duration of action.
Conversely, drugs like erythromycin, cimetidine, and anti-fungal drugs like ketoconazole that inhibit hepatic metabolism, may slow the onset, lower the activity, and/or increase the duration of action of ORLAAM. Caution and close observation of patients receiving these drugs are advised to allow early detection of any need to adjust the dose or dosing interval.
Due to its potential for serious and possibly life-threatening, proarrhythmic effects, LAAM should be reserved for use in the treatment of opiate-addicted patients who fail to show an acceptable response to other adequate treatments for opiate addiction, either because of insufficient effectiveness or the inability to achieve effective dose due to intolerable adverse effects from those drugs (see
WARNINGSand Contraindications ). Cases of QT prolongation and serious arrhythmia (torsade de pointes) have been observed during post-marketing treatment with ORLAAM. Based on these reports, all patients should undergo a 12-lead ECG prior to administration of ORLAAM to determine if a prolonged QT interval (QTc greater than 430 [male] or 450 [female] ms) is present. If there is a prolonged QT interval, ORLAAM should NOT be administered. For patients in whom the potential benefit of ORLAAM treatment is felt to outweigh the risks of potentially serious arrhythmias, an ECG should be performed prior to treatment, 12-14 days after initiating treatment, and periodically thereafter, to rule out any alterations in the QT interval. ORLAAM should be administered with extreme caution to patients who may be at risk for development of prolonged QT syndrome (e.g., congestive heart failure, bradycardia, use of a diurectic, cardiac hypertrophy, hypokalemia, or hypomagnesemia). ORLAAM is metabolized to active metabolites by the cytochrome P450 isoform, CYP3A4. Therefore, the addition of drugs that induce this enzyme (such as rifampin, phenobarbital, and phenytoin) or inhibit this enzyme (such as ketoconazole, erythromycin, and saquinavir) could increase the levels of parent drug or its active metabolites in a patient that was previously at steady-state, and this could potentially precipitate serious arrhythmias, including torsade de pointes (see PRECAUTIONS |
CONDITIONS FOR DISTRIBUTION AND USE OF ORLAAM (42 CFR Part 8)ORLAAM, used for the treatment of opiate addiction, shall be dispensed only by Opioid Treatment Programs (OTPs) certified by SAMHSA under 42 CFR Part 8, and registered by the Drug Enforcement Administration under 21. U.S.C. 823(g)(1). This does not preclude the maintenance or detoxification treatment of a patient who is hospitalized for medical conditions other than opiate addiction and who requires temporary maintenance for concurrent opiate addiction during the critical period of the patients hospitalization. Failure to abide by these requirements may result in injunction precluding operation of the program, revocation of the program approval, and possible criminal prosecution. ORLAAM has no recommended uses outside of the treatment of opiate addiction. |
Administration of ORLAAM on a daily basis has led to excessive drug accumulation and risk of fatal overdose.
ORLAAM has only been studied on a thrice-weekly or every-other-day dosing regimen.
Any decision to administer ORLAAM more frequently than every other day for any reason should be approached with extreme caution. Even then only very small doses (5 to 10 mg) should be considered.
Analysis of some of the deaths from overdose observed in the development of ORLAAM has shown that when ORLAAM is diverted into channels of abuse, the uninformed addict can become impatient with the slow onset of ORLAAM (2 to 4 hours) and take illicit drugs, resulting in a potentially lethal combined overdose when the peak ORLAAM effect develops. Due to these risks of diversion and accidental death, ORLAAM has been approved for use only when dispensed by a licensed facility.
ORLAAM has been shown to prolong the ST segment of the electrocardiogram in beagle dogs dosed five days a week, and to inhibit the rapidly-activating delayed rectifier current I Kr in isolated myocytes in vitro . Serial EKGs performed in a human pharmacokinetics study showed a prolongation of the QTc interval in some patients which was not associated with dose.
Cases of QT prolongation and severe arrhythmias (torsade de pointes) have been observed during post-marketing treatment with ORLAAM. Based on these reports, all patients should undergo a 12-lead ECG prior to administration of ORLAAM to determine if a prolonged QT interval (QTc greater than 430 [male] or 450 [female] ms) is present. If there is a prolonged QT interval, ORLAAM should NOT be administered. For patients in whom the potential benefit of ORLAAM treatment is felt to outweigh the risks of potentially severe arrhythmias, an ECG should be performed prior to treatment and 12-14 days after initiating treatment, and periodically thereafter to rule out any alterations in the QT interval.
ORLAAM should be administered with extreme caution to patients who may be at risk for development of prolonged QT syndrome (e.g., congestive heart failure, bradycardia, use of a diuretic, cardiac hypertrophy, hypokalemia, or hypomagnesemia).
ORLAAM is metabolized to active metabolites by the cytochrome P450 isoform, CYP3A4. Therefore the addition of drugs that induce this enzyme (such as rifampin, phenobarbital, and phenytoin) or inhibit this enzyme (such as ketoconazole, erythromycin, and saquinavir) could increase the levels of parent drug or its active metabolites in a patient that was previously at steady-state, and this could potentially precipitate severe arrhythmias, including torsade de pointes (see
In an individual receiving ORLAAM, the administration of the usual dose of a narcotic antagonist may precipitate an acute withdrawal syndrome. The severity of this syndrome depends on the dose of the antagonist administered and the patient’s level of physical dependence. Narcotic antagonists should be used in patients receiving ORLAAM only if needed. If a narcotic antagonist is used to treat respiratory depression in the physically dependent patient, it should be administered with care and titration should begin with much smaller-than-usual doses (0.1 to 0.2 mg recommended). If the desired effect is not achieved, escalating doses may be administered every 2 to 3 minutes. If a cumulative dose of 10 mg of naloxone has been given without effect, further administration is unlikely to be of benefit (see OVERDOSAGE ).
If the patient does respond to narcotic antagonists, physicians should remember that naloxone has a much shorter duration of action than ORLAAM. Such patients should remain under prolonged observation rather than being allowed to leave emergency treatment, since ORLAAM’s action will outlast naloxone-induced reversal, putting the unsupervised patient at risk of relapse, a return of respiratory depression and possible death if continuing medical attention is not available. Use of other parenteral opioid antagonists may be appropriate in some cases, but only if the dosage of such drugs can be readily titrated. Oral naltrexone would not be appropriate for the treatment of ORLAAM overdose, as it has been associated with the precipitation of prolonged opioid withdrawal symptoms when used in overdose settings.
| Patients must be warned that the peak activity of ORLAAM is not immediate, and that use or abuse of other psychoactive drugs, including alcohol, may result in fatal overdose, especially with the first few doses of ORLAAM, either during initiation of treatment or after a lapse in treatment.
Cases of QT prolongation and serious arrhythmia (torsade de pointes) have been observed during post-marketing treatment with ORLAAM. If a patient taking ORLAAM experiences symptoms suggestive of an arrhythmia (such as palpitations, dizziness, lightheadedness, syncope, or seizures), that patient should seek medical attention immediately. |
Suicide attempts with opiates, especially in combination with tricyclic antidepressants, alcohol, and other CNS active agents, are part of the clinical pattern of addiction. Although outpatient therapy with ORLAAM and other drugs of this class is usually associated with a reduction in the risk of suicide, such risk is not eliminated. Individualized evaluation and treatment planning, including hospitalization, should be considered for patients who continue to exhibit uncontrolled drug use and persistent high-risk behavior despite adequate pharmacotherapy.
Due to the long half-lives of ORLAAM and its metabolites, patients will not feel the full effects of the medication for at least several days. Consequently, extra care is needed when starting patients on ORLAAM and when making initial dosage adjustments (see INDIVIDUALIZATION OF DOSAGE and DOSAGE AND ADMINISTRATION ).
Initiation of therapy or excessive doses of ORLAAM may impair the mental and/or physical abilities required for performance of potentially hazardous tasks, such as driving a car or operating machinery. Patients should be warned not to engage in such activities if their alertness and behavior are affected. Most patients show no detectable impairment of ordinary tasks on ORLAAM therapy.
The respiratory depressant effects of narcotics and their capacity to elevate cerebrospinal fluid pressure may be markedly exaggerated in the presence of increased intracranial pressure. Furthermore, narcotics produce side effects that may make it difficult to evaluate the clinical course of patients with head injuries. In view of LAAM’s profile as a mu agonist, it should be used with extreme caution and only if deemed essential in such patients.
ORLAAM, as with other opioids, should be used with caution in patients with asthma, in those with chronic obstructive pulmonary disease or cor pulmonale, and in individuals with a substantially decreased respiratory reserve, preexisting respiratory depression, hypoxia, or hypercapnea. In such patients, even usual therapeutic doses of narcotics may decrease respiratory drive while simultaneously increasing airway resistance to the point of apnea.
Opioids should be given with caution and at reduced initial dose in certain patients, such as the elderly or debilitated and those with significant hepatic or renal dysfunction, hypothyroidism, Addison’s Disease, prostatic hypertrophy, or urethral stricture.
As with other mu agonists, treatment with ORLAAM may obscure the diagnosis or clinical course in patients with acute abdominal conditions.
No interaction studies have been performed in humans. ORLAAM is metabolized by the cytochrome P450 isoform, CYP3A4. The addition of drugs that induce this enzyme could increase the levels of active metabolites in a patient that was previously at steady-state.
Potentially Arrhythmogenic Agents Any drug known to have the potential to prolong the QT interval should not be used together with ORLAAM. Possible pharmacodynamic interactions can occur between ORLAAM and potentially arrhythmogenic agents such as class I or III antiarrhythmics, antihistamines that prolong the QT interval, antimalarials, calcium channel blockers, neuroleptics that prolong the QT interval, and antidepressants
Caution should be used when prescribing concomitant drugs known to induce hypokalemia or hypomagnesemia as they may precipitate QT prolongation and interact with ORLAAM. These would include diuretics, laxatives and supraphysiological use of steroid hormones with mineralocorticoid potential.
Polydrug and Alcohol Abusers Patients who are known to abuse sedatives, tranquilizers, propoxyphene, antidepres-sants, benzodiazepines, and alcohol should be warned of the risk of serious overdose if these substances are taken while on ORLAAM maintenance.
Interaction with Narcotic Antagonists, Mixed Agonists/Antago-nists, Partial Agonists, and Pure Agonists As with other mu agonists, patients maintained on ORLAAM may experience withdrawal symptoms when administered pure narcotic antagonists, such as naloxone, naltrexone, and nalmefene, or when administered mixed agonists/antagonists or partial agonists such as pentazocine, nalbuphine, butorphanol, and buprenorphine.
In addition, agonists such as meperidine and propoxyphene, which are N-demethylated to long-acting, excitatory metabolites, should not be used by patients taking ORLAAM because they would be ineffective unless given in such high doses that the risk of toxic effects of the metabolites becomes unacceptable.
Anesthesia and Analgesia Patients receiving ORLAAM will develop a similar level of tolerance for opioids as patients receiving methadone. Anesthetists and other practitioners should be prepared to adjust their management of these patients accordingly.
Other Drug Interactions The anti-tuberculosis drug rifampin has been found to produce a marked (50%) reduction in serum methadone levels, leading to the appearance of symptoms of withdrawal in well-stabilized methadone maintenance patients. Similar effects on serum methadone levels have been observed for carbamazepine, phenobarbital, and phenytoin. The presumed mechanism for this effect is the induction of methadone metabolizing enzymes. Since ORLAAM is metabolized into a more active metabolite, nor-LAAM, administration of these drugs may increase ORLAAM’s peak activity and/or shorten its duration of action.
Conversely, drugs like erythromycin, cimetidine, and anti-fungal drugs like ketoconazole that inhibit hepatic metabolism, may slow the onset, lower the activity, and/or increase the duration of action of ORLAAM. Caution and close observation of patients receiving these drugs are advised to allow early detection of any need to adjust the dose or dosing interval.
Patients should be provided the patient package insert for ORLAAM if they are new to the drug, and in addition should be advised that:
ORLAAM, unlike methadone, is not to be taken daily, and daily use of the usual doses will lead to serious overdose.
If a patient taking ORLAAM experiences symptoms suggestive of an arrhythmia (such as palpitations, dizziness, light-headedness, syncope, or seizures), that patient should seek medical attention immediately.
ORLAAM is slow acting and patients should be alerted to the risk of abusing any psychoactive drug, including alcohol, while on ORLAAM therapy. This is particularly important during the first 7 to 10 days of treatment, before ORLAAM has had time to exert its full pharmacologic effect.
In addition to being warned of the delay in onset of ORLAAM, patients who are transferring from ORLAAM to methadone should be informed that they should wait 48 hours after the last dose of ORLAAM before ingesting their first dose of methadone or other narcotic (see DOSAGE AND ADMINISTRATION ).
Patients should inform their adult family members that, in the event of overdose, the treating physician or emergency room staff should be told that the patient is being treated with ORLAAM, a long-acting opioid which is likely to outlast naloxone-induced reversal and which requires prolonged observation and careful monitoring. In addition, the treating physician or emergency room staff should be informed that the patient is physically dependent on narcotics and that naloxone should be administered with care so as to minimize any precipitated abstinence syndrome.
As with most mu agonists, ORLAAM may interact with other CNS depressants and should be used with caution, and in reduced dosage, in patients concurrently receiving other narcotic analgesics, antihistamines, benzodiazepines, phenothiazines or other major tranquilizers, anxiolytics, sedative-hypnotics, tricyclic antidepressants, and other CNS depressants, including alcohol. Patients should be warned of the importance of reporting the use of any of these compounds to their physicians, as serious side effects could result, including respiratory depression, hypotension, profound sedation or coma.
Two-year carcinogenicity studies with LAAM in rats at 13 mg/kg (77 mg/m 2 ) and in mice at 30 mg/kg (90 mg/m 2 ) given orally in the diet did not show carcinogenic changes. LAAM is not mutagenic in the Ames test, the unscheduled DNA synthesis and repair test, mouse lymphoma cells in vitro, or chromosomal aberration tests in rats in vivo. LAAM tested positive in the forward mutation assay in N. crassa at 150 µg/mL in vitro and in the heritable translocation assay in mice at 21 mg/kg (63 mg/m 2 ). The clinical significance of these findings is not known.
Chronic treatment with LAAM at 80 mg three times a week did not produce chromosomal aberrations in peripheral human lymphocytes. Effects of LAAM on fertility in animals has not been fully evaluated.
Animal reproduction studies are not complete and there are no clinical data on the safety of ORLAAM in pregnancy. For these reasons, ORLAAM is not recommended for use in pregnancy. Women who may become pregnant should be advised of the risks of ORLAAM therapy and of the desirability of discontinuing ORLAAM prior to a planned pregnancy.
If a female patient becomes pregnant on ORLAAM despite these precautions, it is recommended she be transferred to methadone for the remainder of the pregnancy (see TRANSFER FROM ORLAAM TO METHADONE , in DOSAGE AND ADMINISTRATION ). If it appears wiser to continue a specific patient on ORLAAM, the physician should be alert to possible respiratory depression of the newborn and other perinatal complications (see Labor and Delivery ).
The effects of ORLAAM on labor and delivery are not known. Like other mu agonist opioids, however, ORLAAM is expected to produce respiratory depression and a possible neonatal dependence syndrome with a delayed emergence of withdrawal symptoms. Use of ORLAAM in labor and delivery is not recommended unless, in the opinion of the treating physician, the potential benefits outweigh the possible hazards.
The effects of LAAM on infants of nursing mothers have not been studied. It is not known if LAAM is excreted in human milk in sufficient concentration to affect an infant. Use of ORLAAM in nursing mothers is not recommended unless, in the opinion of the treating physician, the potential benefits outweigh the possible hazards.
The use of ORLAAM in addicts under 18 years of age has not been studied. Its use is not recommended.
All but a few cases of ORLAAM overdose have involved multiple drugs. Overdose on ORLAAM alone is rare and has always been the result of too frequent (daily) dosing. Overdose is primarily of concern in persons not tolerant to opiates, since in such individuals a dose of 20 to 40 mg of ORLAAM may cause somnolence, and a larger initial dose may cause serious overdose. Tolerant individuals will generally not show symptoms unless higher doses are administered.
In ORLAAM overdose, as with other mu agonist opioids, the following signs and symptoms should be anticipated: respiratory depression (decrease in respiratory rate and/or tidal volume, Cheyenne-Stokes respiration, cyanosis), extreme somnolence progressing to stupor or coma, maximally constricted pupils, skeletal muscle flaccidity, cold and clammy skin, bradycardia, and hypotension. In severe overdose, apnea, circulatory collapse, pulmonary edema, cardiac arrest and death may occur.
In the case of ORLAAM overdose, protect the patient’s airway and support ventilation and circulation. Absorption of ORLAAM from the gastrointestinal tract may be decreased by gastric emptying and/or administration of activated charcoal. (Safeguard the patient’s airway when employing gastric emptying or administering charcoal in any patient with diminished consciousness). Forced diuresis, peritoneal dialysis, hemodialysis, or charcoal hemoperfusion are unlikely to be beneficial for ORLAAM overdose due to its high lipid solubility and large volume of distribution.
In managing ORLAAM overdose, the physician should consider the possibility of multiple drugs, the interaction between drugs, and any unusual drug kinetics in the patient. Naloxone may be given to antagonize opiate effects, but the airway must be secured as vomiting may ensue. If possible, naloxone should be titrated to clinical effect rather than given as a large single bolus, since rapid reversal of opioid effects by large naloxone doses can cause severe precipitated withdrawal effects that may include cardiac instability. If a patient has received a total of 10 mg of naloxone without clinical response, the diagnosis of opioid overdose is unlikely.
If the patient does respond to naloxone, the physician should remember that the duration of ORLAAM activity is much longer (days) than that of naloxone (minutes) and repeated dosing with or continuous intravenous infusion of naloxone is likely to be required. Use of oral naltrexone in this setting is not recommended because it may precipitate prolonged opioid withdrawal symptoms (see Use of Narcotic Antagonists ).
ORLAAM is contraindicated in patients with known or suspected QT prolongation (QTc interval greater than 430 [male] or 450 [female] ms). This would include patients with congenital long QT syndrome, or conditions which may lead to QT prolongation (see WARNINGS, Effects on Cardiac Conduction ) such as: 1) clinically significant bradycardia (less than 50 bpm), 2) any clinically significant cardiac disease, 3) treatment with Class I and Class III anti-arrhythmics, 4) treatment with monoamine oxidase inhibitors (MAOI’s), 5) concomitant treatment with other drug products known to prolong the QT interval (see PRECAUTIONS , Drug Interactions ), and 6) electrolyte imbalance, in particular hypokalemia and hypomagnesemia.
ORLAAM is contraindicated in patients with known hypersensitivity to LAAM.
ORLAAM is not recommended for any use other than for the treatment of opioid dependence (see WARNINGS ).
LAAM is a synthetic opioid agonist with actions qualitatively similar to morphine (a prototypic mu agonist) and affecting the central nervous system (CNS) and smooth muscle. Principal actions include analgesia and sedation. Tolerance to these effects develops with repeated use. An abstinence syndrome generally occurs upon cessation of chronic administration similar to that observed with other opiates, but with slower onset, more prolonged course, and less severe symptoms.
LAAM exerts its clinical effects in the treatment of opiate abuse through two mechanisms. First, LAAM cross-substitutes for opiates of the morphine-type, suppressing symptoms of withdrawal in opiate-dependent individuals. Second, chronic oral administration of LAAM can produce sufficient tolerance to block the subjective „high“ of usual doses of parenterally administered opiates.
LAAM is metabolized by N-demethylation to nor-LAAM and dinor-LAAM, which are also opioid agonists. These metabolites are more potent than the parent drug. The opioid effect which occurs when LAAM is administered is slower in onset and longer in duration (72 hours) than that of methadone (24 hours). This extended duration of action allows three-times-weekly administration (see CLINICAL TRIALS ).
The duration of action of a single dose of LAAM is due to the sum of the opioid activity of the parent drug and its metabolites. A single dose of orally administered LAAM has an onset of opioid effects averaging 2 to 4 hours after ingestion and a duration of action of 48 to 72 hours (as measured by pupillary constriction and suppression of abstinence signs). LAAM cross-substitutes for opiates like morphine in opiate-dependent individuals, suppressing symptoms of withdrawal from these compounds. Single oral doses of 30 to 60 mg of LAAM eliminate signs of abstinence for 24 to 48 hours in individuals maintained on high doses of morphine who are abruptly withdrawn. At higher doses (80 mg and above), suppression of withdrawal can increase to 48 to 72 hours in most individuals.
Repeated oral administration of LAAM can produce sufficient tolerance to block the effects of parenterally administered opiates. Chronic oral administration of 70 to 100 mg of LAAM three times weekly produces tolerance which blocks the „high“ of a 25 mg dose of intravenously administered heroin for up to 72 hours; maintenance on lower doses (50 mg) of LAAM produces only partial blockage for the same period.
LAAM is rapidly absorbed from an oral solution. Plasma levels are detectable within 15 to 30 minutes after ingestion and reach their peak within 1.5 to 2 hours at steady-state. LAAM undergoes first-pass metabolism to its demethylated metabolite nor-LAAM, which is sequentially N-demethylated to dinor-LAAM. Both metabolites are active and contribute to the extent and duration of ORLAAM’s clinical activity (see PHARMACODYNAMICS ).
The steady-state pharmacokinetics of LAAM were modeled from a study in 25 healthy adult addicts using three-times-a-week dosing over a 15-day observation period. LAAM and its metabolites were found to follow a multi-compartment model with extensive tissue distribution (Vd ~ 20 L/kg). LAAM had a clearance of about 0.22 L/kg/hr, mostly by conversion to nor-LAAM. Kinetic studies of the pure metabolites in man have not yet provided accurate estimates of their clearance in the absence of the precursor, but the half-lives observed in this study were 2.6 days for LAAM, approximately 2 days for nor-LAAM, and approximately 4 days for dinor-LAAM.
The pharmacokinetic model used to estimate steady-state plasma levels for each subject in this study assumed a common 3 mg/kg/wk dosage regimen (0.94 mg/kg on Mon. and Wed., 1.125 mg/kg on Fri.). The estimates (which fit the observed data with a correlation of better than 0.95) revealed a large inter-patient variability. There was at least a 5-fold range in peak plasma concentrations for LAAM and its metabolites across the 25 subjects over the 72-hour interval from Friday to Monday on a 3-times-a-week dosage regimen. Table 1 contains these estimates of peak and trough plasma concentrations of LAAM, nor-LAAM, and dinor-LAAM.
| LAAM Mean (CV) |
Nor-LAAM Mean (CV) |
Dinor-LAAM Mean (CV) |
|
|
Cmax(ng/mL) *
|
204 (34%) | 173 (34%) | 114 (28%) |
|
Cmin(ng/mL) **
|
36 (62%) | 85 (58%) | 96 (34%) |
| *Following Friday Morning Dose | |||
| **Prior to Monday Morning Dose | |||
The cyctochrome P450 isoform, CYP3A4, plays a major role in the metabolism of LAAM. As noted above, the formation of nor-LAAM and dinor-LAAM is by sequential demethylation, such that dinor-LAAM is formed from nor-LAAM, not directly from LAAM. While N-demethylation is the primary route of metabolism, minor pathways of elimination include direct excretion and deacetylation to methadol, nor-methadol, and dinor-methadol.
Gender An analysis of the data from the above study showed some difference in the plasma clearance of LAAM in 8 females versus 17 males. Males showed a trend toward a slower conversion of LAAM to nor-LAAM, which may alter the plasma concentration profile of LAAM and its active opioid metabolites. Although this effect was much smaller than the observed inter-individual differences, physicians should be alert to a possible gender difference (see INDIVIDUALIZATION OF DOSAGE ).
Hepatic and Renal Disease At the present time no pharmacokinetics studies have been carried out in subjects with clinically significant hepatic insufficiency or serious renal impairment. Since both the pharmacokinetics and pharmacodynamics of opiate agonists may be altered in these subjects, and any additional risks of ORLAAM therapy are not well understood in such patients, physicians may choose to manage such patients with methadone due to its simpler metabolic profile.
ORLAAM has been studied in 2666 street addicts and 3319 methadone maintenance patients, including 5697 males and 288 females. During the course of 27 studies, 4610 patients received orally administered ORLAAM for up to three years in thrice-weekly doses ranging from 10 to 140 mg. Twenty-one studies provide the primary evidence upon which the dosing recommendations for ORLAAM are based.
The vast majority of patients who received ORLAAM were treated on a thrice-weekly basis, typically on Mondays, Wednesdays and Fridays (Mon./Wed./Fri.), although every-other-day dosing schedules were used in some settings. Most of the sites dosing patients with LAAM on a 3-times-a-week (Mon./Wed./Fri. or Tues./Thurs./Sat.) schedule increased the dose prior to the 72-hour inter-dose interval by 20 to 40% to obtain coverage for the full 72 hours.
In controlled clinical trials, treatment with ORLAAM was found to be comparable to treatment with methadone with respect to reduction in use of illicit opioids. ORLAAM doses in the range of 60 to 100 mg 3-times-a-week reduced the average frequency of urine samples positive for opiates to 15-20%, as did therapy with 50 to 100 mg a day of methadone. There was a trend for more patients to drop out of ORLAAM therapy than methadone therapy in the first 4 weeks of treatment (16% dropouts for ORLAAM v. 12% for methadone), but the dropout rates for both treatments rapidly declined and both were in the range of 1 to 2% per week for the remaining patients by the third month of the studies. Global ratings of patient acceptability and response to treatment were similar for both LAAM and methadone.
In the Phase III studies, ORLAAM tended to be more effective in patients perceived by staff to benefit from a reduced frequency of clinic visits and less effective in patients perceived as needing the added support of daily clinic visits.
Four independent studies were concerned with other research objectives, including induction regimens, methadone-to-ORLAAM (and ORLAAM-to-methadone) crossover ratios, and detoxification. This research involved 800 adults (including 11 females), approximately 440 of whom were methadone maintenance patients. The results of these studies, as well as the results of a nationwide Phase III usage study of 623 patients (including 204 females) in 25 representative clinics across the country, are reflected in the dosing recommendations.
ORLAAM is intended for use as part of a comprehensive treatment plan for narcotic dependence of the opioid type. Supplying narcotic drugs to narcotic addicts for the treatment of addiction without appropriate medical evaluation, treatment planning, and counseling has not been shown to be effective, and is a violation of the law except in special circumstances.
The therapeutic goal early in treatment with ORLAAM is to reduce illicit opioid use. The dose of ORLAAM should be chosen and adjusted as needed to provide a dose that is high enough to suppress drug withdrawal, illicit drug seeking and usage, and related high-risk behavior. If opioid side effects persist once illicit drug use is controlled, the dose of ORLAAM may require further adjustment later in treatment to minimize adverse effects.
Physicians should be alert to patient differences in levels of opioid tolerance and inter-patient variability in the absorption, distribution and metabolism of both ORLAAM and its metabolites. As with methadone, an important contribution to continued abuse of illicit drugs is an inadequate dose of the treatment medication.
Initial dosage adjustment with ORLAAM is complex due to its delayed onset of action. If the starting dose is too high or if the dose is escalated too rapidly for the patient’s level of tolerance, symptoms characteristic of excessive opioid effect may occur, i.e., poor concentration, sedation, and orthostatic hypotension. Patients should be watched for such symptoms, and the dose should be lowered if they appear. In rare instances, serious symptoms of narcotic overdosage may occur, leading to profound CNS and respiratory depression.
ORLAAM and its metabolites quickly accumulate to toxic levels if the doses intended for 3-times-a-week dosing are given too frequently. The recommended doses are intended for every-other-day or 3-times-a-week dosing and should not be given daily.
The recommended initial dose for patients with low or unknown tolerance to opioids is 20 to 40 mg three-times-a-week or every-other-day. Successive doses may be increased by 5 to 10 mg. At least two weeks are needed to achieve a clinical plateau after a dosage adjustment. Adjustment to a dosing schedule is dependent upon the rate at which an individual develops tolerance to the increasing level of ORLAAM (and its metabolites) as well as the time required for ORLAAM and its metabolites to accumulate to steady-state levels.
The goal of dosage titration is to suppress narcotic withdrawal while avoiding excessive opioid effects due to the build-up of long-acting metabolites. It may be safer to provide extra counseling and support rather than to attempt to completely suppress a patient’s withdrawal or narcotic hunger during the first week or two of therapy. On the other hand, there is the ever-present danger that patients who receive sub-therapeutic starting doses will supplement with street drugs, resulting in overdose. Patients should be strongly warned against this practice. Later in the titration process, dosage adjustments are better made on a weekly basis whenever possible.
For patients on methadone maintenance whose level of tolerance is known, the recommended initial dose of ORLAAM is 1.2 to 1.3 times the patient’s daily dose of methadone, not to exceed 120 mg. Care should be taken not to adjust the dose too frequently thereafter (usually 5 to 10 mg changes every second or third dose) since increasing the dose too rapidly may result in oversedation.
One major advantage of ORLAAM therapy is reduction in need for daily clinic visits and for take-home medication. In some patients, ORLAAM may not provide adequate suppression of withdrawal for a full 72 hours. For such individuals, several therapeutic options are available: (1) extra support and an explanation of reasons for the effect, (2) increasing the dose given prior to the 72-hour interval, (3) switching to an every-other-day dosing schedule, (4) dispensing a supplemental methadone dose.
Most patients do not experience withdrawal during the 72-hour inter-dose interval after reaching pharmacological steady-state with or without adjustment of the Friday dose. If additional opioids are required, and the patient is not eligible or appropriate for take home doses of ORLAAM, small doses of supplemental methadone should be given rather than giving ORLAAM on two consecutive days. Take-home doses of ORLAAM and methadone always pose a risk in this setting and physicians should carefully weigh the potential therapeutic benefit against the risk of diversion (see DOSAGE AND ADMINISTRATION ).
Patients should receive extra support and counseling and be warned against supplementing with street drugs as they make the switch from methadone to ORLAAM. The variability in the clearance of LAAM, nor-LAAM, and dinor-LAAM and clinical experience suggest that there will be a small number of patients who require either lower or higher doses than those recommended.
There is no information from controlled clinical trials as to the appropriate duration of ORLAAM therapy. There are reports from investigators that some patients on ORLAAM may experience less variation in opioid effects and have less drug craving than with methadone, so ORLAAM should be considered for patients who need long-term maintenance during social and vocational rehabilitation.
When a patient has eliminated illicit drug use, achieved social and occupational stability, and made lifestyle changes to reduce the risk of relapse, consideration may be given to discontinuation of ORLAAM therapy. Such a decision should be carefully considered as part of an individualized treatment plan. Stable long-term ORLAAM therapy is preferable to repeated cycles of premature discontinuation of medication followed by relapse to uncontrolled addiction.
A patient is most likely to remain abstinent if discontinuation of medication is attempted after the achievement of behavioral objectives and is accompanied by appropriate non-pharmacological support. The rate of dose reduction should vary according to patient’s response. Discontinuation of ORLAAM therapy for administrative reasons or because of adverse reactions to the drug should be managed as described below under DOSAGE AND ADMINISTRATION .
Patients should be provided the patient package insert for ORLAAM if they are new to the drug, and in addition should be advised that:
ORLAAM, unlike methadone, is not to be taken daily, and daily use of the usual doses will lead to serious overdose.
If a patient taking ORLAAM experiences symptoms suggestive of an arrhythmia (such as palpitations, dizziness, light-headedness, syncope, or seizures), that patient should seek medical attention immediately.
ORLAAM is slow acting and patients should be alerted to the risk of abusing any psychoactive drug, including alcohol, while on ORLAAM therapy. This is particularly important during the first 7 to 10 days of treatment, before ORLAAM has had time to exert its full pharmacologic effect.
In addition to being warned of the delay in onset of ORLAAM, patients who are transferring from ORLAAM to methadone should be informed that they should wait 48 hours after the last dose of ORLAAM before ingesting their first dose of methadone or other narcotic (see DOSAGE AND ADMINISTRATION ).
Patients should inform their adult family members that, in the event of overdose, the treating physician or emergency room staff should be told that the patient is being treated with ORLAAM, a long-acting opioid which is likely to outlast naloxone-induced reversal and which requires prolonged observation and careful monitoring. In addition, the treating physician or emergency room staff should be informed that the patient is physically dependent on narcotics and that naloxone should be administered with care so as to minimize any precipitated abstinence syndrome.
Wolstein J, Gastpar M, Finkbeiner T, Heinrich C, Heitkamp R, Poehlke T, Scherbaum N.
Department of Psychiatry and Psychotherapy, Rhine State Hospital, University of Duisburg-Essen, Essen, Germany.
INTRODUCTION: Levo-Alpha-Acetylmethadol (LAAM) is a synthetic opioid analgesic with mu-agonistic activity and a long duration of action. There are several, almost exclusively US American studies showing the efficacy of LAAM as a maintenance drug which has the advantage that it needs to be administered only three times a week. LAAM is currently not marketed in EU countries due to cardiac complications. We report on the first European multi-center, parallel group, flexible dose, open-label, randomized clinical trial comparing LAAM and methadone in patients with opioid dependence.
METHODS: Eighty-four opioid addicts in ongoing maintenance treatment with stable methadone doses were treated with methadone under study conditions for 5 weeks (run-in phase), then randomly assigned to a methadone (n=41) or a LAAM (n=43) group. Study duration was 24 weeks after randomization. Objective measures (drug urine screenings, retention rate), subjective measures (symptoms of withdrawal and craving, report of substance use), and safety data were collected weekly. The main outcome criterion was the number of opiate-free urine samples per number of weeks of study participation.
RESULTS: Non-inferiority was shown for LAAM compared to methadone. Both substances were well tolerated. There were no clinical cardiac complications in either group.
DISCUSSION: Our study confirmed the results of previous investigations with LAAM as being efficacious and well tolerated in opioid dependence. A discussion to reconsider the availability of LAAM is recommended.
This paper is the twenty-ninth consecutive installment of the annual review of research concerning the endogenous opioid system, now spanning thirty years of research. It summarizes papers published during 2006 that studied the behavioral effects of molecular, pharmacological and genetic manipulation of opioid peptides, opioid receptors, opioid agonists and opioid antagonists. The particular topics that continue to be covered include the molecular-biochemical effects and neurochemical localization studies of endogenous opioids and their receptors related to behavior (Section 2), and the roles of these opioid peptides and receptors in pain and analgesia (Section 3); stress and social status (Section 4); tolerance and dependence (Section 5); learning and memory (Section 6); eating and drinking (Section 7); alcohol and drugs of abuse (Section 8); sexual activity and hormones, pregnancy, development and endocrinology (Section 9); mental illness and mood (Section 10); seizures and neurological disorders (Section 11); electrical-related activity and neurophysiology (Section 12); general activity and locomotion (Section 13); gastrointestinal, renal and hepatic functions (Section 14); cardiovascular responses (Section 15); respiration and thermoregulation (Section 16); and immunological responses (Section 17).
2. Endogenous Opioids and Receptors
Morphine administered systemically or directly into the ACC produced a naloxone-sensitive reduction in pain affect, as demonstrated by decreased aversiveness of noxious cutaneous stimulation in nerve-damaged animals with no concomitant alteration of response to mechanical stimulation (623). NAC morphine-induced increases in thermal and mechanical hindpaw latencies were blocked by naloxone, BFNA and NBNI, but not NTI (1244). Morphine in the thalamic nucleus submedius reduced the second phase of formalin-induced evoked spinal dorsal horn nociceptive responses in a naloxone-reversible manner (1317). Microinjections into the thalamic nucleus submedius of morphine, endomorphin-1 or DADL, but not the kappa agonist, spiradoline, dose-dependently inhibited mechanical and cold allodynia induced by spinal nerve ligation, effects blocked by general and mu, but not delta antagonism (1187). Similarly, microinjections into the ventrolateral orbital cortex of morphine, endomorphin-1 or DADL, but not the kappa agonist, U-62066, dose-dependently inhibited mechanical and cold allodynia induced by spinal nerve ligation, effects blocked by general and mu, but not delta antagonism (1318).
Morphine, gabapentin and lamotrigine produced analgesia of similar potencies in attenuating capsaicin and nerve-injury-induced mechanical hypersensitivity (535). Morphine modulated potentiation of capsaicin-evoked TRPV1 responses through a cyclic AMP-dependent PKA pathway (1160). Intrathecal naloxone or CTAP blocked systemic morphine- and fentanyl-induced analgesia on mechanical measures of nociception as well as thermal responses to the hindpaw, but not forepaw (198). However, noncompetitive interactions between the opioid antagonists, CTAP and naltrexone were observed in the rat tail-withdrawal assay (1175). Morphine-associated pruritus occurred after a single extradural injection in a horse (150).
Two studies independently demonstrated that morphine-induced decreases in intraocular pressure and pupil diameter in rabbits was blocked by naloxone and partially reversed by L-NAME or L-glutathione, indicating NO involvement (111, 296). Low-dose morphine-induced hyperalgesia was blocked by PLC inhibitors (U73122) and blockers (calphostin C), also by ketamine and MK-801, and finally by AS against PLCbeta3 (378). Acute and chronic morphine increases Phase II pain-associated behaviors on the formalin test in neonatal rats after four days of abstinence (1332).
The analgesic efficacy of such partial opioid agonists as buprenorphine or tramadol was increased in mice with targeted inactivation of the alpha2A-adrenoceptor gene or in wild-type mice treated with atipamezole and yohimbine (874). Tramadol produced analgesia in MOR KO mice that was blocked by alpha-2 adrenergic antagonists alone or with naloxone, but not by methysergide (499). Isobolographic analysis revealed dual-site synergism in the systemic and intraplantar antinociceptive response of tramadol in the formalin test in rats (921). Oral and intrathecal, but not ventricular oxycodone, but not morphine produced analgesia in diabetic mice. Whereas, mu but not kappa or delta antagonism blocked oxycodone analgesia in non-diabetic mice, kappa, but not mu or delta antagonists blocked oxycodone analgesia in diabetic mice (852). Whereas subcutaneous oxycodone and oxymorphone produced potent analgesia in the hot-plate and paw pressure tests, intrathecal oxymorphone produced far more potent effects than intrathecal oxycodone (645). Liposome-encapsulated hydromorphone provided extended analgesia in a rat model of neuropathic pain (1047). Analgesic effects were observed after epidural administration of hydromorphone in horses (822), and similar effects were observed following subarachnoid hyperbaric morphine, buprenorphine and methadone (823). Systemic and intrathecal remifentanil produced naltrexone-reversible analgesia on the acetic acid test in Rana pipiens (792). Gabapentin activated the NO-cyclic GMP-K+ channels pathway in inhibiting formalin-induced pain (869). Spinal alpha-2 adrenergic and muscarinic receptors as well as the NO release cascade mediated the supraspinally-produced effectiveness of gabapentin in decreasing mechanical hypersensitivity in mice after partial nerve injury (1103).
In preparation for a trial on co-prescription of heroin to chronic treatment-resistant addicts, a pharmaceutical dosage form for smokable heroin was developed. During development of this product (a mixture of diacetylmorphine and caffeine), in vitro experiments were performed simulating ‚chasing the dragon‘: the technique used by addicts for inhalation of heroin after volatilisation. Samples were heated on aluminium foil using a heating device and the vapours were collected and analysed using a HPLC-UV method. The recovery of diacetylmorphine and caffeine in vapours was studied after volatilisation of different powder mixtures at temperatures between 200 and 350 degrees C. Furthermore, the volatilisation set-up was combined with an Andersen sampler to determine the sizes of aerosol particles. Only small differences in recovery of diacetylmorphine and caffeine were found between temperatures and between powder mixtures: 46-62% of diacetylmorphine from the sample was recovered in vapour and 65-83% of caffeine. The only degradation product detected in vapour was 6-acetylmorphine (4.1-7.1%). In the temperature range studied, temperature mainly influenced the volatilisation rate. Mass median aerodynamic diameters of aerosols from diacetylmorphine-containing samples ranged from 1.8-4.1 microm; 45-60% of each sample was recovered as aerosol particles <5 microm. Volatilising pharmaceutical smokable heroin resulted in sufficient amounts of diacetylmorphine in vapour and in particles suitable for effective deposition in the lungs.
Pharmaceutical heroin for inhalation was developed for a clinical trial on co-prescription of heroin and methadone to chronic treatment-resistant heroin addicts. Diacetylmorphine base was selected as the active pharmaceutical ingredient for this product with caffeine anhydrate added as an excipient. Differential scanning calorimetry and thermogravimetric analysis showed that addition of caffeine resulted in a lower melting temperature and a higher volatilisation rate for the mixture than for diacetylmorphine base alone. Recovery experiments showed that 40.8+/-5.3% of diacetylmorphine base could be found in smoke condensate after volatilisation of diacetylmorphine-caffeine tablets. All of the caffeine from each tablet was recovered unchanged in the fumes, while 85.6% of the diacetylmorphine from each tablet was recovered, either unchanged in the fumes or as non-volatilised residue. Recovery was found to be reproducible and only small differences were found between the tablet types. The experimental set-up was found to efficiently collect the vapours resulting from heating the powder. Under the tested experimental conditions, no evidence was found that degradation products of diacetylmorphine or caffeine, other than 6-acetylmorphine (5.9%) had volatilised, even though a decomposed residue was present after heating diacetylmorphine-caffeine samples. Diacetylmorphine-caffeine was found to be a suitable basis for pharmaceutical heroin to be used by ‚chasing the dragon‘.
In diacetylmorphine prescription programs for heavily dependent addicts, diacetylmorphine is usually administered intravenously, but this may not be possible due to venosclerosis or when heroin abuse had occurred via non-intravenous routes. Since up to 25% of patients administer diacetylmorphine orally, we characterised morphine absorption after single oral doses of immediate and extended release diacetylmorphine in 8 opioid addicts. Plasma concentrations were determined by liquid chromatography-mass spectrometry. Non-compartmental methods and deconvolution were applied for data analysis. Mean (±SD) immediate and extended release doses were 719 ± 297 mg and 956 ± 404 mg, with high absolute morphine bioavailabilities of 56% to 61%, respectively. Immediate release diacetylmorphine caused rapid morphine absorption, peaking at 10 to 15 min. Morphine absorption was considerably slower and more sustained for extended release diacetylmorphine, with only ~30% of maximal immediate release absorption being reached after 10 min and maintained for 3 to 4 h, with no relevant food interaction. The relative extended to immediate release bioavailability was calculated to be 86% by non-compartmental analysis and 93% by deconvolution analysis. Thus, immediate and extended release diacetylmorphine produce the intended morphine exposures. Both are suitable for substitution treatments. Similar doses can be applied if used in combination or sequentially.
Opioid misuse and addiction embody a grave public health issue. Treatment in most countries is primarily based on methadone and buprenorphine maintenance programs (Van den Brink and Haasen, 2006, Amato et al., 2005). However, treatment response is often incomplete, and many heavily dependent narcotic addicts cannot be included or retained in these programs. Therefore, Switzerland and several other countries now include diacetylmorphine as an additional option for heavily dependent narcotic addicts (Fischer et al., 2007, van den Brink et al., 2003, Sheldon, 2008, Haasen et al., 2007, Brissette, 2001). Based on the three most relevant clinical studies in Switzerland, the Netherlands, and Germany, heroin-assisted treatment is superior to other opiod-assisted treatments such as methadone (Rehm et al., 2001, van den Brink et al., 2003, Haasen et al., 2007, Verthein et al., 2008). In particular, this treatment targets previously untreated intravenous drug users or non-responders to conventional methadone treatments, who subsequently show improvements in health status, often dramatically, less treatment dropout, reduced consumption of other psychotropic substances, and other social improvements. Based on these successful study outcomes, the Swiss and the Dutch health authorities have registered an intravenous diacetylmorphine formulation, and oral formulations have been submitted in Switzerland for marketing approval. In addition, other countries such as Spain, Belgium, Denmark, Canada, and the United Kingdom are planning or have already completed clinical trials with heroin-assisted treatments.
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Figure 1
In vitro diacetylmorphine dissolution profiles of immediate and extended release tablets
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Table 1
Pharmacokinetic comparison of oral immediate (IR) and extended (ER) release diacetylmorphine.
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Figure 2
Individual morphine plasma concentration–time profiles after orally administered immediate (A) and extended release diacetylmorphine in the fasted (B) and the fed (C) state
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Figure 3
Goodness-of-fit plots for immediate (A) and extended release diacetylmorphine in the fasted (B) and the fed (C) state from deconvolution analysis using a bi-exponential disposition and a linear spline absorption function
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Table 2
Absolute and relative bioavailability estimates for immediate (IR) and extended release (ER) diacetylmorphine from the deconvolution analysis in NONMEM and their 90% and 95% confidence intervals.
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Auswirkungen von Drogen auf Menstruation, Schwangerschaft, Geburt und Kindesentwicklung
Opiate haben neben vielfältigen Wirkungen auch neuroendokrine Effekte. Sie führen u.a. zu einer Abnahme des luteinisierenden Hormons (LH) und des Follikel-stimulierenden Hormons (FSH). Die Prolaktinspiegel steigen dagegen an.
Die Gonadotropine LH und FSH werden im Hypophysenvorderlappen gebildet. Erniedrigte Werte bei Heroinabhängigkeit, Anorexie und durch Einnahme von Ovulationshemmern
Diese hormonellen Effekte sind zusammen mit psychosozialen Stressfaktoren dafür verantwortlich, dass viele abhängige Frauen an Amenorrhoe oder Oligomenorrhoe leiden.
Unter oral eingenommenen Substituten mit langsamerer Anflutungsgeschwindigkeit als bei i.v. oder nasal eingenommenem Heroin kommt es meist zu einer Normalisierung der Menstruation.
Ein Opioid induzierter Östrogenmangel kann langfristig zu einer Osteoporose führen.
Bei Frauen, die Drogen nehmen, ist die Schwangerschaft mit besonderen Risiken verbunden. Dies gilt für legale wie für illegale Drogen. Das ungeborene Kind ist an den Blutkreislauf der Mutter angeschlossen. Konsumiert eine schwangere Frau Drogen, können diese auf das Kind übergehen. Das Kind kann dadurch schwere, z.T. auch lebenslange Schäden davontragen. Es gibt bei den Drogen/Alkohol/Medikamenten keine Dosis, die eventuell toleriert werden kann. Bei Opiaten wie Heroin ist allerdings dringend zu empfehlen auf ein Substitut umzusteigen.
Die Risiken des Nikotin Konsums:
20 % der Schwangeren rauchen. Auswirkungen sind fetale Wachstumsverzögerung, Spontanabort, Tabakentzugssyndrom, plötzlicher Kindstod. Die Ursache ist wahrscheinlich die erhöhte Kohlenmonoxidbelastung. 30 Zigaretten/ Tag führen zu einer 60% Reduktion der fetalen Sauerstoffversorgung. Die Kinder wiegen bei Geburt im Durchschnitt 200gr. weniger.
Sie haben auch ein erhöhtes Risiko für die spätere Entwicklung einer Leukämie.
Die Risiken des Alkohol Konsums:
Alkohol gelangt über die Nabelschnur rasch in den Blutkreislauf des ungeborenen Kindes, und verbreitet sich im ganzen Körper. In ganz kurzer Zeit haben Mutter und Kind denselben Alkoholspiegel.
Die schädigende Wirkung des Alkohols hält aber beim ungeborenen Kind länger an, als bei der Mutter, weil der noch nicht vollständig entwickelte Organismus Alkohol sehr langsam abbaut. Die Blutalkoholspiegel sind nach Konsum eine Zeit lang deutlich höher, als bei der Mutter.
Alkohol hat beim Feten eine teratogene Wirkung. In hohen Dosen (tägl.> 60gr) kann es zum fetalen Alkoholsyndrom (FAS) kommen, dazu gehören Wachstumsverzögerung, Gesichtsmissbildungen wie Lippen-, Kiefer-, Gaumenspalte, Herzfehler, Funktionsstörungen des ZNS , motorische und intellektuelle Fehlentwicklungen, die zu lebenslangen Beeinträchtigungen führen können. Es gibt aber auch bei geringerem Alkohol Konsum auch „leichtere“ Verhaltensauffälligkeiten und intellektuelle Beeinträchtigungen, die dann oft nicht auf den Alkohol Konsum in der Schwangerschaft zurückgeführt werden.
Die Risiken des Cannabis Konsums:
Untersuchungen zeigen, dass die Schadstoffaufnahme eines Joints, etwa der von 5 Zigaretten entspricht. Der Konsum von THC führt zu einer deutlichen Reduktion des Geburtsgewichts.
Es gibt nur wenige Untersuchungen, aber Hinweise, dass es später zu Verhaltensauffälligkeiten kommen kann. Diskutiert werden auch Sprach-, Gedächtnis-; und Lernstörungen. Die Wahrscheinlichkeit einer Risikoschwangerschaft ist erhöht, da THC die Einnistung des Embryos in die Gebärmutter verhindern kann.
Die Risiken des Kokain Konsums:
Die gefäßverengende Wirkung des Kokains hat Durchblutungsstörungen der Gebärmutter und der Plazenta zur Folge. Dadurch wird das werdende Kind schlechter mit Sauerstoff und Nährstoffen versorgt, es kann zu einer vorzeitigen Placenta Ablösung (Fehlgeburt) und vorzeitigen Wehen kommen (Frühgeburt).
Kokain passiert die Plazentaschranke und führt zu einer 4 x höheren Konzentration, verglichen mit der Schwangeren.
Es kommt gehäuft zu Missbildungen vor allem im Urogenitaltrakt und zu Schädigungen der neuronalen Entwicklung. Postpartal zeigen die Kinder häufig Anzeichen der Neurotoxizität, wie Zittrigkeit, erhöhte Irritabilität, aber auch Lethargie und erhöhtes Schlafbedürfnis.
Die Risiken des Amphetamin und Ecstasy Konsums:
Amphetamine bewirken einen erhöhten Gefäßtonus mit Hypertonie und Tachykardie und als Folge eine fetale Mangelversorgung (s.Kokain). Es besteht die Gefahr einer Fehl- o. Frühgeburt, und eines geringeren Geburtsgewichtes.
Es gibt Hinweise auf eine erhöhte Rate von Fehlbildungen.
Die Risiken des Benzodiazepin Konsums:
Es gibt Hinweise auf vermehrte Fehlbildungen im Bereich des Gesichtes, Lippen-Kiefer-Gaumenspalten, besonders wenn Benzodiazepine im ersten Trimenon konsumiert werden. Ebenso Herz- und Gefäßmissbildungen, und geistige Entwicklungsverzögerungen.
Neugeborene zeigen bei Benzodiazepin – Konsum der Mutter das am längsten dauernde und intensivste Entzugssyndrom (NAS) mit starkem Zittern, anhaltender Nervosität, leichter Irritierbarkeit, Blutdruckkrisen, Temperaturabfall, Erbrechen, Durchfall usw. Der Entzug von Benzodiazepinen kann länger als 4 Wochen dauern, und mit epileptischen Anfällen einhergehen.
Die Risiken des Opiat Konsums:
Opiate wie Heroin gehen direkt in den Blutkreislauf des Kindes über. Nach bisherigen wissenschaftlichen Erkenntnissen haben sie keine teratogen, d.h. fruchtschädigenden Wirkungen. Die Risiken fürs Kind sind aber niedriges Geburtsgewicht und Frühgeburten. Ist das Straßenheroin mit Streckmitteln wie Diazepam u.a. versetzt bestehen hier weitere Risiken.
Besonders gravierend ist das neonatale Abstinenzsyndrom (NAS), das bei Heroin 24-48 Stunden nach der Geburt auftritt, und mehrere Wochen dauern kann.
Therapie der Wahl ist die Substitution mit synthetischen Opioiden, nicht nur zur Verhinderung von Entzugserscheinungen, Vermeidung von Rückfällen und Zusatzkonsum, sondern auch zur gesundheitlichen und zur sozialen Stabilisierung.
Die Dosis sollte ausreichend sein. Im dritten Trimenon kommt es durch Enzyminduktion zu einem erhöhten Bedarf. Dosiserhöhung u.o. Dosissplitting kann notwendig sein.
In 60 – 80 % kommt es nach der Geburt zu einem neonatalen Entzugssyndrom, das nach heutigen Erkenntnissen bezgl. Dauer und Ausprägung unabhängig von der Dosis des Substituts ist. Subutex scheint günstiger zu sein, das NAS schwächer und kürzer, allerdings ist die Datenlage bezgl. Methadon/Polamidon besser.
Die Behandlung des NAS sollte mit oralen Morphinen erfolgen, nicht mit Barbituraten.
Cable dated:2006-05-23T11:49:00
C O N F I D E N T I A L SECTION 01 OF 03 PHNOM PENH 000983
SIPDIS
SENSITIVE
SIPDIS
STATE FOR EAP/MLS, INL/AAE–PETER PRAHAR AND YANTI KAPOYOS, INL/C–GREG STANTON
E.O. 12958: DECL: 05/23/2016
TAGS: SNAR, PGOV, CB, TW
SUBJECT: CAMBODIA: DRUG SEIZURES AND ARRESTS UP
1. (U) SUMMARY: May 19 and 20 arrests of two Taiwanese nationals attempting to smuggle a total of nearly 7 kg of heroin to Taiwan highlight increased drug arrests and seizures in Cambodia. The quantity of heroin seized during the weekend airport busts is large by Cambodian standards–authorities seized just 11 kg of heroin in 2005. Seizures of amphetamine-type stimulants are more than double last year’s levels. Police and international observers credit USG and other foreign training with providing skills, motivation, and international pressure for the increase, but say that narcotics trafficking may also be on the rise. END SUMMARY.
Heroin Seizures at Phnom Penh International Airport
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2. (U) Police and customs officials seized nearly 7 kg of heroin and arrested three Taiwanese nationals in two separate incidents at Phnom Penh International Airport on May 19 and 20. These two cases represent an impressive intake for one weekend given that in 2005 Cambodian authorities seized just over 11 kg of heroin.
3. (SBU) Chen Hsin Hung, 57, was arrested on May 19 carrying 4.75 kg of heroin with a local street value of USD 95,000 to 133,000. Customs officials became suspicious when they noticed that Hung was carrying several bags of imported Taiwanese foil-wrapped candies back to Taiwan in his hand luggage. The candies turned out to be foil-wrapped packages of heroin. Hung, who was due to travel to Taiwan via Kuala Lumpur on Malaysian Airlines flight 755, had arrived in Phnom Penh the previous day. During his police interrogation, Hung said that he had been picked up at the airport and returned to the airport by a couple, whom the police identified as a Cambodian woman and a mainland Chinese or Taiwanese man. Police are attempting to locate the couple.
4. (SBU) A second Taiwanese man, who was standing near Chen Hsin Hung during the security process, appeared to be quite interested in the proceedings and upset by Hung’s arrest, and had tickets for the same flight as Hung, was also arrested on suspicion of drug trafficking. Moek Dara noted that the investigation had revealed no evidence to indicate that the second individual was also involved in drug smuggling, but that it was the prosecutor’s decision how to proceed in the case.
5. (SBU) On May 20, a 90-year-old Taiwanese national named Huang Sang Hou was arrested at Phnom Penh International Airport with 1.9 kg of heroin, worth USD 38,000 to USD 53,000. Hou reportedly came to Cambodia as a tourist intending to gamble. Over the course of a week, he lost the USD 4,000 he brought with him, borrowed an additional USD 2,000 from a Taiwanese national in Phnom Penh, and then lost that money as well. The Taiwanese lender then persuaded Hou to carry the heroin back to Taiwan. Airport customs officials were tipped off by the sloppy manner in which the heroin was packed on Hou’s body, making him appear bloated. Hou cooperated with the police in identifying the Taiwanese lender, and Cambodian government officials have already passed his name, address, and passport information to the Drug Enforcement Administration (DEA). Hou had been planning to fly Dragon Airlines flight 207 to Hong Kong, and then to continue on to Taiwan.
Amphetamine Seizures, Prices on the Rise
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6. (SBU) According to statistics from the Ministry of Interior’s Anti-Drug Police and the National Authority for Combating Drugs (NACD), seizures of amphetamine-type stimulant (ATS) tablets more than doubled when comparing the first four months of 2006 with the first four months of 2005. From January to April 2006, more than 220,000 ATS tablets were seized, whereas from January to April 2005, approximately 87,000 ATS tablets were seized. The number of offenders arrested also rose from 154 from January to April 2005 to 204 during January to April 2006.
7. (U) Both Brigadier General Moek Dara, Director of the Anti-Drugs Department, and World Health Organization XXXXXXXXXXXX noted that prices for ATS tablets have risen in the past few years, with particularly dramatic increases in the past 12 months. One year ago, a single ATS tablet sold for approximately one dollar in Phnom Penh, but now costs two to three dollars. Moek Dara noted that prices rise as the ATS tablets make their way along the drug route, from fifty cents per tablet in Laos, where the
PHNOM PENH 00000983 002 OF 003
majority are produced, to USD 3 in Cambodia, and then even higher prices in two destination countries: USD 4 in Vietnam and USD 7.50 in Thailand. XXXXXXXXXXXX cited anecdotal evidence from NGOs that some ATS users are switching to injecting heroin, currently available for USD 1.50 to 2 in Phnom Penh, as a cheaper alternative to rising ATS prices.
Lower Ecstasy Seizures Likely Point to Disrupted Network ——————————————— ———–
8. (U) In contrast to the dramatic rise in ATS seizures, seizures of ecstasy tablets are down sharply, from 1,900 in January to April 2005 to less than 800 in January to April 2006. Moek Dara and XXXXXXXXXXXX believe that lower levels of ecstasy seizures are a sign that supply has been disrupted following a cooperative DEA/Anti-Drug Police controlled delivery operation against the Peter Brown drug ring in 2004 and continued Anti-Drug Police action against the ring in 2005.
USG Training Provides Needed Skills, International Pressure
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9. (SBU) Moek Dara gave much of the credit for the dramatic increase in heroin and ATS seizures and drug arrests to counternarcotics training funded by the State Department’s Bureau of International Narcotics and Law Enforcement Affairs (INL) and conducted by the DEA. Before the training sessions, which were conducted in January and April 2006, police officers along Cambodia’s porous northern border were not very active and would not even conduct foot patrols in the forest, according to Moek Dara. Now, however, the officers have more skills and are more motivated to patrol actively, he said, and have seized drugs and a lot of drug production equipment as well. Customs, immigration, and police officials at the airports are also better trained and more active, and Moek Dara noted that all of the officials involved in the weekend’s airport arrests had completed DEA training.
10. (C) XXXXXXXXXXXX gave partial credit for increased anti-drug activity to counternarcotics training by the US and other foreign donors. Some high-ranking Cambodian police and military officials are rumored to be complicit in narcotics trafficking, he noted. He speculated that the training and pressure on the Cambodian government to clamp down on drug activity has finally made an impression on higher ranking officials, and lower-level officers are „being allowed“ to make more seizures. At the same time, such a dramatic increase is probably also an indication of efforts to traffic increased amounts of ATS through Cambodia, he opined.
Trainees Enthusiastic about INL/DEA Courses
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11. (U) Provincial Anti-Drug Police officers who attended the January Basic Counternarcotics course reported uniformly enthusiastic assessments to an embassy follow-up survey. Participating police captains reported an increased awareness of drug smuggling tactics, best practices in seizing and preparing evidence, and how to identify drugs using field test kits. Captain Preap Sovann of the Svay Rieng Anti-Drug Police noted that the training also promoted inter-agency and inter-province cooperation as well. All captains reported training their staffs in the key topics covered by the DEA training, and captains in Koh Kong and Pursat provinces reported conducting anti-drug outreach to primary and secondary school students as well. Trainees suggested that future courses provide written materials in Khmer as well as English, include information on money laundering, have more laboratory equipment available for in-class practice in drug identification, and include more time in simulations.
Police Officer Arrested on Drug Charges
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11. (C) Nov Sophal, a municipal police officer in the southern city of Kep, was arrested on April 15 and charged with trafficking 1 kg of heroin. Moek Dara was not expansive when asked about the case, noting simply that it is not uncommon for low-ranking police and military officials to be arrested for drug trafficking. In contrast, XXXXXXXXXXXX noted that drug investigations of police or military officials are very rare, and speculated that the individual involved may even have run afoul of rumored higher-level police involvement in narcotics.
12. (SBU) COMMENT: While increased smuggling activity may
PHNOM PENH 00000983 003 OF 003
account for some of the increased seizures and arrests, it is clear that the Cambodian government is turning up the heat on the country’s drug smugglers. Training from the USG and other countries is playing a critical role in supporting this effort–both through the skills and enthusiasm imparted to the participants, and also through the implicit expectations of improved performance on the part of the police and other officials.
STORELLA
source: http://www.guardian.co.uk/world/us-embassy-cables-documents/65065
MOSCOW — They look like addicts anywhere in the world: tattered and vacant-eyed, they circle Moscow pharmacies known to sell prescription drugs illicitly, looking for something to inject for a quick high.
Pyotr Nikitenko, right, distributed medical supplies and literature outside a pharmacy in Moscow with a drug outreach center colleague, left. Mr. Nikitenko, a former heroin user, said most of his friends were now H.I.V. positive.
Though public examples of Russia’s problem with heroin are not new and seldom bring even raised eyebrows among locals, the issue has recently come to symbolize a broader failure. The country has become one of the world’s low points in the effort to fight the spread of H.I.V., and unchecked intravenous drug use is the biggest cause, international health officials say.
The epidemic here has defied worldwide trends, expanding more rapidly year by year than almost anywhere else. Nearly 60,000 new cases of H.I.V., the virus that causes AIDS, were documented in Russia in 2009, an 8 percent increase from 2008, according to Unaids, the United Nations H.I.V./AIDS program. Of those new cases, more than 60 percent were believed to have been caused by intravenous drug use, and many of the others were believed to have been infected through sex with addicts.
Though South Africa, with more infections than any other country, far outstripped that total number, with an estimated 390,000 new infections in 2009, the rate of new infections annually has decreased there by nearly half since its peak in the late 1990s.
“I’ve been researching the problem of H.I.V. infection for 25 years, and I must say that the situation has become significantly worse” in Russia, said Dr. Vadim V. Pokrovsky, the head of the country’s Federal AIDS Center.
While in recent years the government has increased its efforts to fight the disease, Dr. Pokrovsky said, current programs almost completely neglect those groups at the heart of it.
Officials estimate that well over a million people abuse drugs intravenously in Russia, often sharing and infecting one another with tainted needles. They are among Russian society’s most marginalized people, more likely to face a few weeks handcuffed to a clinic bed than to receive basic treatment to break their addictions. Meanwhile, officials have treated sex education and other preventative programs with open hostility.
“Which are the main infected groups? Injecting-drug users and sex workers,” said Lev Zohrabyan, the Europe and Central Asia adviser for Unaids. “It turns out that these are the groups where the money must be directed to change the picture. But if you open the budget, you will see that for prevention work among these groups for the next two years there is nothing.”
Top officials have consistently blamed the United States’ failure to eradicate heroin production in Afghanistan for Russia’s intravenous drug problem. About 90 percent of Russian addicts use Afghan heroin, according to the Federal Drug Control Service.
Yet once the drugs pass through Russia’s porous borders with former Soviet republics in Central Asia, dealers find a ready market of addicts with few tools to help them quit. While some regions have experimented with needle-exchange programs, the practice, which has proven effective at reducing the spread of H.I.V. in other countries, has not been adopted on a national level.
The country’s top medical and political officials have roundly condemned drug substitution therapy for heroin addicts — the use of methadone or other narcotics, widely considered an effective way to wean people off the drug — on the basis that it substitutes one form of addiction for another. Doctors who have flouted the official ban on the treatment have faced prosecution and even harassment by Kremlin-backed youth groups.
The Russian Orthodox Church, which has become a significant voice in the country’s political affairs in the past decade, has also expressed strong opposition to such preventative measures.
Even a new antinarcotics strategy ordered by President Dmitri A. Medvedev last summer acknowledges Russia’s failure to adequately confront the problem. “Prophylactic activities, medical aid and rehabilitation of patients with drug addiction are not sufficiently effective,” said the document, posted on Mr. Medvedev’s Web site.
Many of the addicts gathered outside one pharmacy in southern Moscow said they had often tried to stop. “You want to quit, and you don’t,” said a graying 33-year-old named Maxim who had the scarred arms of a dedicated user. Another man, who had quarter-size holes gouged into his body from injection-related infections and would not give his name, said he feared that he would be arrested if he sought treatment — a worry that is not completely unfounded here.
The police often arrest drug users, sending them to special detoxification centers where doctors encourage, and sometimes force, immediate abstinence, which can in some rare cases be fatal. Last summer, organizers of the 18th annual International AIDS Conference held in Vienna issued a declaration — aimed at Russia and the countries of the former Soviet Union, in particular — arguing that such practices drove addicts underground, complicating H.I.V.-prevention efforts.
It is not that the government has failed completely to recognize the gravity of the epidemic. Russia’s national security strategy, approved by Mr. Medvedev, identifies the spread of H.I.V. and AIDS as “one of the main threats to national security in the sphere of medicine and health.”
Russia now has more than 500,000 officially registered cases of H.I.V., though Unaids and other experts have estimated the actual number to be closer to one million, as many as in the United States, which has more than twice the population.
Part of the problem is that the government came late to the fight. The epidemic has been raging since the Soviet collapse two decades ago, but a major government response came only in 2006 when Russia’s obligations as host of the Group of 8 summit meeting pushed officials to take a more active role in fighting the disease. Vladimir V. Putin, who was president at the time and is now prime minister, ordered the largest increase in financing in any area in Russia’s history, and spending has grown annually ever since.
This year, the government plans to nearly double spending on H.I.V. drugs to about $600 million and expand prevention programs focusing on youth, said Galina G. Chistyakova, a Health Ministry official who helps oversee Russia’s H.I.V. and AIDS policies. She denied that Russia was having trouble curbing the epidemic, noting that the ministry had documented a slight dip in the number of new infections in 2010 compared with a year earlier.
Dr. Pokrovsky and others said that government programs often became ensnared in Russia’s large and inefficient bureaucracies. Even efforts to provide AIDS patients with treatment, which constitute the bulk of government financing, have fallen short.
Patients and doctors have complained of frequent shortages of antiretroviral drugs to the point where patients have created online communities, like pereboi.ru, that monitor drug deficits and help those in need of medicines connect with people who have extra supplies. Patients have also held street protests, and others have sued.
Many addicts who become infected do not even know that medicines are available, said Pyotr Nikitenko, 28, a former heroin user who now works for a Moscow-based outreach group called Yasen. He said he was able to wean himself off heroin with the help of his family, escaping the fate of most of his friends, who he said now were H.I.V. positive.
“I continue to bury them,” Mr. Nikitenko said. “They continue to die from AIDS, or rather they are dying more and more frequently.”
Russia has one of the fastest spreading HIV epidemics in the world, driven largely by the government’s refusal to institute measures to treat the country’s drug addicts — measures that have dramatically reduced HIV infections in drug addicts in other countries, including the U.S.
The New York Times reported yesterday that 60,000 new cases of HIV were seen in Russia in 2009, up 8% from the prior year. At least 60% of those new cases were spread by intravenous drug use, according to the Times, and a good portion of the rest of the new cases were likely the result of sex with drug addicts. (More on Time.com: Drug Policy Backfires: Controlling Meth Ingredients Fails to Cut Drug Supply)
Writes the Times‘ Michael Schwirtz:
Officials estimate that well over a million people abuse drugs intravenously in Russia, often sharing and infecting one another with tainted needles. They are among Russian society’s most marginalized people, more likely to face a few weeks handcuffed to a clinic bed than to receive basic treatment to break their addictions. Meanwhile, officials have treated sex education and other preventative programs with open hostility.
“Which are the main infected groups? Injecting-drug users and sex workers,” said Lev Zohrabyan, the Europe and Central Asia adviser for Unaids. “It turns out that these are the groups where the money must be directed to change the picture. But if you open the budget, you will see that for prevention work among these groups for the next two years there is nothing.”
According to Schwirtz, Russia blames America’s failure to eradicate Afghanistan’s opium crops for the IV drug problem in Russia. But if the U.K.’s current shortage of heroin, due to Afghan crop failures this year, are any indication, the international heroin supply has actually been significantly reduced. Regardless, changes in the supply side have never had any impact on the HIV epidemic.
So, what’s really driving Russia’s problem? Politics. The country has a long-standing ideological opposition to the use of “substitute” maintenance drugs like methadone and buprenorphine to treat IV drug addicts. Yet methadone is the best known treatment for heroin addiction: according to numerous reviews of the voluminous international data, it reduces relapse and death rates better than any other treatment, including all therapies based on abstinence. The effectiveness of buprenorphine treatment for heroin addiction is also well-supported by research. (More on Time.com: Salvia, a Mexican Hallucinogen Piques Scientists‘ and Regulators‘ Interest)
In all countries that have successfully reduced HIV infection rates among intravenous drug users, health officials have instituted maintenance treatment programs. But they have all also simultaneously increased clean-needle availability — the other public-health measure that undergirds many effective AIDS-prevention programs. In that respect, Russia has not been entirely remiss: it does offer some needle-exchange programs that provide addicts with clean syringes and educate them not to share.
Alone, methadone maintenance programs and legal needle-and-syringe exchanges cannot stop an epidemic. But the evidence is pretty clear that together, they can. Case in point: New York City.
In the not too distant past, New York was the epicenter of the AIDS epidemic among America’s drug addicts. In the early 1990s, at least half of all intravenous drug users in the city were HIV-positive. But a recent study of HIV infection rates among injected-drug users in New York found that while 21% of addicts tested positive for HIV between 1984 and 1994, that figure dropped to just 6% in people who used IV drugs between 1995 and 2008.
What changed? The two groups are distinguished by the prevention measures most available to them. In the 1980s and early ’90s, New York City had a large methadone treatment system, but awareness of the spread of HIV among drug addicts was initially low; at the time, syringe exchange programs were also either illegal or just getting started, and needle possession was illegal. (More on Time.com: The Most Dangerous Drugs? Alcohol, Heroin and Crack — in That Order)
In 1992, needle exchanges were legalized in New York City, and massively expanded by 1995. Over-the-counter sales of syringes in New York became legal in 2001.
Nationally, the AIDS epidemic in addicts has subsided too, with only 12% of new cases linked to IV drug use, down from more than 1 in 3.
Given that the data overwhelmingly show that maintenance programs and needle exchanges, together, can significantly reduce the spread of HIV, Russia’s refusal to treat the country’s million-plus drug users is putting millions more of its citizens — including nonusers who may be partners of drug users or of infected former partners — at deadly risk.
Swat raids and paramilitary civilian police forces threaten our beliefs and our way of life.
In the United States many people still believe that our homes are private and as such should be free from government intrusion. Further many believe we have the right to defend our home and family from unlawful intruders and that the constitution guarantees this. After all we fight wars in the name of freedom and protecting our god-given as well as civil rights even now. It appears we are in danger of losing our fourth amendment rights, and once gone they may be gone forever.
The implications for Americans are huge. For some time now we have seen increasing use of militarized SWAT teams across the country invading American homes, even killing our citizens and their pets on what looks to be the flimsiest of excuses many times. Countless innocent people have been killed or injured during these raids.
According to the New York Times,
“More than 60 years ago, the Supreme Court ruled that the police were not entitled to enter a residence without a warrant merely because they smelled burning opium, this has been the law of the land since.”
The Supreme Court of the United States recently took up the issue in arguments of a case about what the police were entitled to do upon smelling marijuana outside a Kentucky apartment. Concerns have been raised and there is a very real possibility that the court may be poised to vacate the previous ruling, requiring police to get a search warrant before entering our homes.
“Aren’t we just simply saying they can just walk in whenever they smell marijuana, whenever they think there’s drugs on the other side?” said Justice Sonia Sotomayor during the recent arguments. “Why do we even bother giving them a warrant?”
The current precedent requiring search warrants was established by the Court in 1948 with Johnson v. United States: The smell of opium is insufficient cause to enter a premises without a search warrant.
Justice Jackson delivered the opinion of the court: “No reason is offered for not obtaining a search warrant except the inconvenience to the officers and some slight delay necessary to prepare papers and present the evidence to a magistrate. These are never very convincing reasons and, in these circumstances, certainly are not enough to bypass the constitutional requirement. ”
There are literally thousands of militarized raids every year (perhaps as many as 40,000). Even when police get a search warrant which is not very difficult these days they often misrepresent the facts or raid the wrong house terrorizing innocent families including children like this case in Spring Valley New York last week.
Police Terrorize 13-Year-Old Girl In Botched Pot Bust.
Police conducting drug raids early in the morning woke a family dragging them out bed, even pointed a machine gun at a 13-year-old girl and threatened to shoot the family poodle…..one big problem and this happens often in these full military type raids they had the wrong house and the wrong family. Luckily this time no one was killed but many other times the innocent victims of the police raid were not so lucky. Here is a list of a few of those not so lucky victims of police para military raids.
In the recent Spring Valley raid, David McKay said “Their guns were drawn, they were screaming ‘Where’s Michael, Where’s Michael. ” At least 10 heavily armed officers had stormed the house at 5:30am. McKay’s daughter was so terrified and traumatized he had to take her to Nyack Hospital, for treatment after she had an asthma attack and fainted following the ordeal.
Mckay is quoted in an article by Radley Balko on January 13 2011.
“They pulled me outside in the freezing cold in my underwear, manhandle my wife, point a gun at my daughter and they won’t even tell me what they are doing in my house,” said McKay. “It was terrifying and humiliating beyond belief.”
Thirteen law enforcement agencies (LEA’s) were involved in the raids. This was just one of the many joint federal/local drug sweeps for pot that occur daily around the U.S. In Hawaii county we recently saw something similar in the coordinated raids again by 13 agencies, against Roger Christie’s THC ministry and the “Green 14″. In that case the government brought in a C-140 Coast Guard cargo plane specifically to whisk the 14 defendants off the Big Island to federal detention in Honolulu.
The amount of money they spend on these raids is hard to pin down but mind boggling when you start adding it up. Christie still has not gotten a trial of any kind yet is being held without bail as a “danger to the community” for a marijuana crime, more than 6 months after police found a measly 2 pounds of marijuana, and $21,000.00.
That’s it – after a 2 year investigation by the 13 law enforcement agencies – at a cost that already runs in the millions of dollars – 2 pounds of marijuana. In the recent New York raid as police were preparing to leave, McKay and his bewildered family asked them again what they were doing and why they entered the house. “They wouldn’t say,” “All they would say was ‘You’ll read about it in the paper tomorrow.’ ”
In the search warrant case now before the U.S. Supreme court, police officers in Kentucky were looking for a suspect who they claim had sold cocaine to an informant. They further claim they smelled burning marijuana coming from an apartment, knocked loudly and announced themselves. That according to an article by Adam Liptak, published January 12, 2011 in the New York Times, and entitled Justices Look Again at How Police May Search Homes.
The article reports that police claim to have heard sounds from inside the apartment, leading them to believe evidence was being destroyed, so they kicked in the door. While they did find marijuana and cocaine, the suspect in the original cocaine case was not there. The Kentucky Supreme Court sided with the defendants and suppressed the evidence. The court found that any risk of drugs being destroyed was the result of the decision by the police to knock and announce themselves rather than to obtain a warrant. Now the state of Kentucky and the federal government want the U.S. Supreme court to overturn Kentucky’s Supreme court ruling. Essentially the government is asking the court to take away the 4th amendment rights of all Americans.
In Mr. Liptak’s article he states Justice Sotomayor was even more direct.
“Aren’t we just doing away with ‘Johnson’?” she asked.
He also points out that Justice Ruth Bader Ginsburg asked why the police could not simply roam the hallways of apartment buildings, sniffing; knock whenever they smell marijuana; then break in if they hear something suspicious. All in all it’s a great article that points out that the other Justices seem inclined to rule in the government’s favor. If that happens we will lose even more of our ever-eroding rights in this country, and can look forward to many more military-style swat raids terrorizing families around the nation.
We continue to see ever increasing militarization of civilian law enforcement in this country, including Hawaii county, where I live. This has led to a dramatic increase in paramilitary police units (SWAT) being used for routine police work. The most common use of SWAT teams today in Hawaii county and around the nation is to serve drug warrants, usually with forced, unannounced entry into our homes. A large number of those raids are for marijuana. Swat was originally brought about to be used in hostage situations, but has been co-opted to gradually militarize civilian police departments over the last few decades. As we see, the result has been the erosion of the civil liberties we enjoy, as we have moved to the point of becoming a virtual police state.
With the ever-increasing numbers of SWAT raids in America, the number of nonviolent drug offenders, innocent bystanders, and wrongly accused U.S. residents, injured or even killed has been rising. The terror of having your homes invaded while sleeping, usually by large teams of heavily armed paramilitary forces, has not escaped even the mayor of the small town of Berwyn Heights MD, very near the capitol of our nation.
A police SWAT team raided the home in 2008, shooting and killing the family’s two dogs. They falsely accused the mayor of receiving 32 pounds of marijuana. Was this military type swat raid necessary? Of course not.
“My government blew through my doors and killed my dogs,” Calvo said. Imagine what they do to people that are not so prominent or god forbid actually guilty of a marijuana crime. Must see articles and video here:
Gung Ho SWAT Team Kills Mayor’s Dogs In Botched Pot Raid
Maryland Mayor’s Dogs Killed During No-Knock Raid
Police shot the families 7-year-old dog Payton, handcuffed the mayor’s mother-in-law (making her lie next to the dead dog on the floor), shot the other 4-year-old dog Chase in the back, and then handcuffed Calvo in only his boxer shorts. Mrs. Calvo said, “They were my kids. All I could see was the blood and the tissue of the dogs”–the police apparently tracked the dogs’ blood through the house. The police claim they had a no-knock warrant, but failed to produce one until 71 hours later according to Mayor Calvo.
The family maintains the two black Labradors were harmless and said police apparently killed them “for sport,” gunning down one of them as it was running away.” “Our dogs were our children.”
Prince George’s County Police Chief Melvin High and other officials refuse to apologize for killing the dogs, maintaining the officers felt threatened (clearly they are in the wrong profession). We all know how scary dogs can be while they’re running away from you. Imagine if the U.S Supreme court rules police really don’t need a warrant what will happen. The only reason we heard about this is because Calvo was the mayor.
This is a much more common occurrence than most people are aware of or would like to believe. These raids are very violent in nature and are used against even nonviolent drug offenders including misdemeanors offenses, as we see many victims of these raids turn out to be completely innocent. It is clear, in many instances the raids terrorize innocents when police mistakenly target the wrong residence or people who’s only crime is being in the wrong place at the wrong time. There have been dozens of needless deaths and injuries, not only of drug offenders, but also of police officers, children, bystanders, and innocent suspects, and those responsible for this are rarely if ever held accountable or brought to justice.
There is no doubt this is happening, the scary part is it’s getting worse as the Kentucky case now at the Supreme Court demonstrates. The government and judicial system are condoning –even supporting– more attacks against us, when the real problem is the failed drug war.
The solution is to review and change the drug laws that are the underlying cause of not only everything in this article, but the majority of the drug abuse in this country. Drugs are a health problem. Criminalizing drugs has manufactured criminals and crime. In business and life the policy is responsible for the results it gets, not so in the war on drugs or it would have ended long ago. Somehow common sense and rational thought do not count when we consider the drug war.
Here are some more very disturbing police abuses that are being condoned and facilitated.
South Dakota School Officials Terrorized Kindergarten Classes with Drug-Sniffing Dogs.
“The very notion of there being a drug problem in the kindergarten is ludicrous.”“
But read what happened, this is your government doing this nobody else. Its even worse as this case has racial overtones and these laws are being used in discriminating manners as this case exemplifies.
A school official who accompanied the police instructed the students to put their hands on their desks and avoid petting or looking at the dog or making any sudden movements. In some classrooms, a school official told students that any sudden movement could cause the dog to attack. Is this what we call a free country now? The drug laws are a bigger problem than the drugs, the police are more dangerous most often than anyone else. In at least one instance, the ACLU complaint said, the dog escaped its leash in a kindergarten class and chased students around the room. Some students had been traumatized by previous dog attacks and one young girl still has the scars of a previous attack on her face. Many began crying and trembling and at least one urinated involuntarily. What lesson did this teach these children?
Again these are just some of the ones you here about, most of them are never reported:
These drug raids are far more dangerous to everyone than marijuana ever could be. In one case Police opened fire with children in the house killing the family dogs in front of those children. It’s a miracle no people were killed. Those children were endangered by the police and traumatized in ways that will be with them the rest of there lives, they did this over marijuana. They could easily have arrested the father away from the home but chose to do it this way because there are no consequences for them.
It’s time to legalize marijuana and put an end to this once and for all. This is not only dangerous and socially destructive to families and the community it is economically unsustainable. Hundreds of billions of dollars are wasted on these raids and laws and look at the results. Look at what we get for that money. We could reduce drug abuse in this country and slice hundreds of billions from our budget while improving the lives of millions of families by simply reforming the laws and the policies of prohibition and treating this like the health problem it is. We could cripple the drug cartels over night, in fact we could hardly have a worse policy if we tried, creating crime and filling our prisons while enriching drug cartels and bankrupting our country. This may go down as the worst policy in American history when we finally wake up to the fact that it is responsible for the mess in which we find ourselves.
The public policy debate on Afghan opium is filled with simple narratives (i.e., it is mostly opium that fuels the insurgency, poppy farmers are wealthy) justified by simple metrics and responded to with simple solutions. The problem with simplicity, of course, is that it crowds out complexity and propels us toward ineffective and even counterproductive policies.
Much of the counternarcotics debate in Afghanistan focuses obsessively on cultivation numbers produced by the United Nations Office on Drugs and Crime’s (UNODC) annual opium survey, with annual changes in cultivated area used as indicators of policy success or failure. Yet such changes are the result of a range of factors, including price shifts, household perceptions of future food insecurity and larger market forces. They are therefore transient, not necessarily indicative of fundamental changes in the rural economy.
For instance, last year’s 22 percent reduction in national opium acreage was largely attributed to the distribution of wheat seed and fertilizer in Helmand Province, which by itself produces around half of Afghanistan’s opium. But this reduction was less the result of policies and programs than farmers‘ rational response to the changing relative prices of wheat and opium. Memories of high wheat prices and concerns over insecurity in central Helmand continue to shape planting decisions, highlighting the fact that farmers give greater priority to managing the risk of food insecurity than to maximizing profits. After all, one can’t eat opium poppy no matter what its price.
The addiction to annual cultivation numbers has similarly produced praise for the firm commitment and strong hand of the provincial governors in Balkh and Nangarhar, the two provinces most lauded for success in becoming „poppy free“ in 2008 (in 2009, some poppy cultivation resumed in Nangarhar). Yet short-term reductions brought about by coercion may not be sustainable, and the side effects include migration to Pakistan (with attendant risk of radicalization), increasing enlistment in the Afghan National Security Forces under duress, sales of household assets and incurring of debt—as well as the potential undermining of support for the national government, which was seen as the driving force behind the coercion.
Fieldwork done in the areas hardest hit by the opium ban in these two provinces reveals a widespread perception that the economic impact on the general population has been too severe and that the social „contract“ under which reductions have been made is breaking down. In fact, one could argue that coercive suppression of cultivation in areas where there are no other viable sources of income is leading to greater instability—and thereby establishing preconditions for increased cultivation. One needs only to look at recent insurgency penetration in a number of districts in Nangarhar to see what appears to be the failure of success.
Some of the narratives analysts use to justify an aggressive approach to opium poppy reduction, including the „nuclear option“ of aerial chemical spraying, are built on „faith-based“ policy and questionable data. Several years ago, for instance, a US military commander mentioned that the percentage of the insurgency funded by the opium trade was likely between 20 and 40 percent, although an „international expert“ had said that the percentage could reach 60 percent; within weeks, much of the media had discarded the caveats so that 60 percent became the number of record. In some counterinsurgency circles, the belief that only 10 percent of the population is directly engaged in cultivation legitimates coercive measures on the grounds that even the harshest approach will not alienate the majority of the population. Yet the figure is based on a flawed methodology, and it ignores both the multiplier effect of the created wealth as well as bonds of solidarity, by which communities will band together to resist outside threats to life and livelihoods.
Such arguments also tend to shift from year to year. In 2007, UNODC proclaimed that „opium cultivation is no longer associated with poverty—quite the opposite.“ But by 2009 it was saying that „opium remains a major source of income in one of the world’s poorest and most unstable countries. Farmers may grow it to stave off poverty…. Eradicate poverty, not just poppies.“
The past two years have brought a welcome respite from the eradication debate, in part because of the Obama administration’s focus on the interdiction of traffickers rather than the destruction of crops, and in part because the military has sensibly recognized that obliterating Afghan rural livelihoods does not win hearts and minds. Still, there are forces that remain committed to a more aggressive eradication strategy, and they may be revived if the number of hectares heads upward in key provinces. If this year’s opium figures show an increase in cultivation, brace yourself for lurid headlines, Congressional delegations and calls to abandon a failed policy.
Rather than constantly alternating between back-slapping and hand-wringing, in the discussion over counternarcotics we should keep in mind that the transition away from opium is a long-term process and that the annual ups and downs are somewhat irrelevant. We must recognize that one size will not fit all areas, and that we can’t simply view drugs as a „bad“ to be stomped out while ignoring the role they play at all levels of the political economy. Ironically, aspects of the opium economy have contributed to stability and development by generating financial flows that have, in turn, been used to fund other licit economic activities, while counternarcotics policies have destabilized areas by forcing households deeper into poverty and by undermining political arrangements.
Above all else, acknowledging that drugs are a part of the rural economy and social structure in the distressed environment of a country wracked by decades of war and violence will allow us to focus on governance, security and economic growth—which will facilitate a slow but steady transition out of opium rather than spending on stovepiped, single-season interventions.
Source: http://www.thenation.com/article/157630/addicted-numbers
SHAN STATE, 13 January 2011 (IRIN) – Poverty and lucrative profits make poppy cultivation increasingly attractive to farmers who would otherwise produce legal crops to feed their families and make a living, say experts.
„More of the rural poor continue to be drawn into participating in the illicit drug trade as a last means of finding money to feed their families,“ Jason Eligh, Country Representative for the UN Office on Drugs and Crime (UNODC) Myanmar, told IRIN.
Shan State, 400km north of the capital, Yangon, between Myanmar, Laos and Thailand, produces more than 90 percent of all opium in Myanmar, an estimated 35,000 tons in 2010, according to UNODC.
UNODC is the only international agency directly involved in supporting different crops in poppy cultivation areas, with three agriculture projects in southern Shan State trying to reach 100,000 people. However, much more needs to be done to stop farmers from reverting to opium production, said Eligh.
„UNODC wants to see a strong alternative development response, one that includes market access, community mobilization, access to credit, improved technology and better overall infrastructure in rural areas.“
Cash crop
In 2010, a higher proportion of farmers‘ income came from poppies than in previous years, reversing a trend of steady decline in the past six years.
Between 2003 and 2009, the proportion of total household income from poppies fell from 70 to 20 percent, according to a December 2010 UNODC report.
In 2010, however, high prices paid for poppy in Myanmar and low food security throughout the country meant income from the seed contributed to 43 percent of total household income in Shan State, the report stated. About a quarter of the state’s population was involved, estimate aid agencies.
Though prices at source (farm-gate) for poppy fell marginally in 2010 from 2009, opium overall remained lucrative at US$305 per kilo. Poppy farmers can earn 13 times more money cultivating poppies than rice, making poppies the cash crop of choice for most, based on the UNODC report.
Farmers forced out of poppy cultivation are having problems growing other food to survive. „I grow enough vegetables to keep my family going, but that is all,“ U Tin Kyi told IRIN.
U Tin Kyi grew poppy seeds to supplement his income until authorities destroyed his fields two years ago. Like many of his neighbours in this hilltop village, U Tin Kyi has little extra income. „The fuel cost to get to the market outweighs any profit I would make from selling vegetables,“ he told IRIN.
Eradication efforts
Poppy cultivation continued to rise in Myanmar in 2010, despite an official 15-year drug elimination plan developed in the late 1990s. In 2009, the authorities initiated the final five-year phase of this plan.
Government figures claim 8,268 hectares of poppy-cultivating land were eradicated in 2010, a 102 percent increase on the previous year.
But other groups calculate that Myanmar’s poppy cultivation area and yield actually increased during this period.
„In 2010 we estimate that there [was] 20 percent more area under opium poppy cultivation, a 46 percent increase in average opium yield, and a 17 percent increase in the number of households involved in domestic opium poppy cultivation,“ said Eligh of UNODC.
In northern Shan State, in 2008, government figures showed 25 percent of poppy fields were destroyed, but a 2010 report by Palaung Women’s Organization (PWO), an NGO based in Mae Sot along the Thai-Myanmar border, stated only 11 percent of poppy fields had been eradicated.
Government anti-drug teams were only destroying easily visible poppy fields and filing false eradication data to the police headquarters, the report said. At the same time, farmers were forced to pay taxes to continue growing poppies.
In Mantong village in northern Shan State, PWO estimated the government collected approximately $37,000 in poppy taxes in 2008.
Summary
Introduction
Methadone detoxification is a complex area dealt with in various sections throughout this book.
This section deals with the practical issues around prescribing and the rate of detox, the anxieties for clients about detox and the alternatives to methadone in detox.
This section should be read in conjunction with:
People reducing from methadone are often anxious and afraid of the withdrawal syndrome and relapse.
Relapse following detox is an often neglected area because drug services and drug users tend to concentrate on the withdrawal syndrome and process of detoxification.
Effective follow up is vital in ensuring that detoxification is more than a reducing dose of methadone mirrored by a concurrent rise in heroin (or other depressant drug) use or a prelude to a short period of abstinence followed by relapse that the prescriber is unaware of.
Information for clients on the issues around detoxification and residential rehabilitation is available in the Detox Handbook and the Rehab Handbook – also available from ISDD (address on back cover).
Reasons for detoxing
In an ideal world people would detox from a stabilising dose of methadone or illicit drugs when they, and their prescriber, agreed that they were ready and able to do so without significant risk of early relapse. However people may want to detox when either they or their prescriber do not feel they are ready because:
These are discussed below.
Attitudes of staff
Opiate users are sensitive to the attitudes of the staff they come into contact with and sometimes choose not to seek, or to terminate treatment because of the attitudes and behaviour of staff.
This can probably be best avoided by offering services that are:
Following these principles also means that, having discussed the options, if a client decides to detoxify against advice the staff should still offer their full support and encouragement during and after the detox. They should also endeavour to discuss possible outcomes in a way that does not set the client up to fail but allows the making of contingency plans that can be brought into play if the detox does not work.
Unrealistic staff beliefs about a client’s ability to detox
It is easy for workers to fall into the trap of prematurely believing that people can achieve abstinence and encourage the client to detox. Often the client will continue down this road because they do not want to upset the worker and this can continue afterwards, with the client not wishing to re-refer themselves to a prescribing service for fear of admonishment from, or upsetting, the people who helped them before.
Cushman and Dole87 found that of a group of methadone maintenance clients who were assessed as ‚rehabilitated‘ and detoxed with the anticipation of success, some asked to be returned to maintenance during the detox and 25% returned to maintenance after detox (mainly because of protracted withdrawals).
Therefore support, encouragement and optimism should always be tempered by continual reassessment and meaningful negotiation.
Unrealistic client beliefs about their ability to detox
Clients too can be unrealistically optimistic about their ability to get off opiates. Often people will present after many years of heavy opiate use, adamant that in a few weeks they will be able to get themselves together and detox successfully.88
This belief sometimes stems from concentrating on the physical aspects of opiate withdrawal. If past experience of relapse during or after opiate detox has been that the withdrawal symptoms were the main factor causing relapse, this can reinforce the belief that if the physical symptoms of withdrawal can be reduced to tolerable levels by a methadone detox, abstinence will be easily achieved.
Another factor can be the flawed but understandable and apparently logical conclusion that ‚if all my problems are heroin-related then if I give up heroin all my problems will go away‘. The experience of many is that the compulsive behavioural aspects of their drug taking and the social and emotional difficulties that they experience once opiate-free add a previously ignored and difficult-to-overcome dimension to their drug use.
Stigma associated with having a methadone prescription
Many people on a maintenance methadone prescribing programme say ‚the act of having to take an opiate every day is a reminder that I’m a junkie‘.
For the relatives and friends of people on methadone it can be perceived as being ‚as bad as heroin‘ – regardless of any associated lifestyle improvements that have been achieved. Indeed associated improvements often serve only to increase the pressure on the person to detox as the perception is that they do not need the methadone anymore.
Heroin users are often dismissive of those on methadone and street myths of the terrible long-term health consequences of methadone treatment still abound. So the person receiving methadone often feels stigmatised from all sides.
Heroin users who feel the need to seek help for the first time also feel this and may request a methadone detox so that they can rationalise their request as one for a short-lived intervention that does not involve long-term methadone treatment.
Dislike of practical aspects of a regime, such as the collection frequency
Avoidance of longer-term treatment may also include factors such as a desire not to have to:
It is important for the worker involved to have an awareness of these issues if they are factors in a request for methadone detoxification.
Change of drug of choice
Sometimes poly drug users change their drug of choice in a cyclical way from, say, heroin to benzodiazepines to alcohol to amphetamines and back to heroin; or simply switch from heroin to, say, alcohol and back again.
They may ask for a detox at the end of the opiate part of the cycle – either as a new referral as a heroin user or following a period on methadone. In these cases treatment may or may not be appropriate, but if commenced should be carefully monitored.
Clients going to prison
Clients who have a prison sentence coming up present drug services with a dilemma. On the one hand premature detox may lead to relapse with risk behaviour prior to prison. On the other hand arriving at a prison where detox facilities are poor or non-existent in full methadone withdrawal is likely to result in illicit heroin use. The sharing of injecting equipment in prison is much more prevalent than in the community. The best that can be done is to:
Blind or open reductions?
There is no evidence to suggest that knowing or not knowing the frequency or size of dose reductions is more effective in helping people detox using methadone.
The answer for most people who attend prescribing and dispensing services that are flexible enough to offer both, is to consider the pros and cons of each approach in conjunction with the prescribing staff, and to make an informed decision for themselves as to which is the most appropriate regime. Generally a key factor is the level of control that a person feels they have over their lives. Anyone who feels in control is unlikely to opt for blind dose reductions.
The arguments for and against blind and open reductions are set out below.
| Arguments for blind dose reductions | Arguments against blind dose reductions |
|---|---|
| Reduced anxiety around the day of dose reduction | Possible constant anxiety about when reductions are going to happen |
| Objective self assessment of withdrawal symptoms | Constant anxiety about and experience of withdrawal symptoms |
| Concentration on issues around coping rather than drug dose | Client not taking responsibility for the dose reductions or their response to them |
| Reduced anxiety about passing psychologically important doses e.g. 20mg,10mg, 5mg | Inability to ‚take credit‘ for success so far |
| Arguments for open dose reductions | Arguments against open dose reductions |
|---|---|
| Client takes responsibility for the dose reductions and their response to them | Increased anxiety and expectations of withdrawal symptoms at times of dose reductions |
| Ability to plan life around reductions | Weeks of concentration on drug dose as the major factor in determining ability to function is not always helpful preparation for a drug-free life |
| The rate of reduction can be negotiated once detox has started | Client is more able to identify psychologically significant doses at which to stop – which can weaken resolve |
Setting the appropriate rate of detox
Almost everyone undergoing methadone detoxification will experience withdrawal symptoms, and for many these will be serious enough to be a major contributing factor in either relapse to heroin use or a request for methadone maintenance – even if all other preconditions for a successful detox are in place.87
For people detoxing following a period on methadone maintenance, faster detoxes are associated with higher drop-out rates and slower detoxes are associated with lower drop-out rates.89
In general detoxes consist of gradual reductions of 5mg or 10mg in the daily dose to a given level, usually 20-30mg (depending on the starting dose and the client), and then become more gradual, either in terms of time between reductions and/or size of daily dose reduction.
Negotiation between worker and client is an important component of any detoxification. A negotiated detoxification in which the client is able to take responsibility for coping with the dose reductions is likely to reduce the risk of concurrent illicit opiate use and be a better foundation for continued abstinence afterwards.
Prescribers without specialist experience who agree to a short-term programme without support from a specialist service should seek support if their patient is unable to detox successfully at the agreed rate.
Detox regime suggestions
All the regimes below are for methadone mixture 1mg/1mL. All detox regimes are a plan only and should be subject to regular, i.e. weekly or fortnightly, review against the treatment aims.
The definitions, indications and contra-indications for each of the regimes below are given in Section 7 – Treatment aims and choices. It is important that detox regimes are only entered into with clear treatment aims and following a thorough assessment that has established that these aims are achievable.
The very low doses (i.e. less than 5mg) suggested in the following regimes are of little physiological value as they are unlikely to make much difference to the level of physical withdrawal. However withdrawal symptoms can also be aggravated by anxiety and where low dose prescribing at the end of a detox reduces anxiety it is likely to reduce subjectively experienced withdrawals.
Where a client has high levels of anxiety about making the final reductions they are often afraid of being drug free and of the changes this will bring. It is therefore important that low dose prescribing is coupled with counselling.
Short-term detoxification: decreasing doses over one month or less Two week detoxification regime
This regime has the advantage that it is easy to prescribe as there is a dose drop at the end of each week.
An alternative starting slightly higher could be:
For people who need more methadone to stabilise or who are detoxing from an existing methadone prescription there are two main choices. Either reduce the dose prior to the final detox or reduce the dose by 25%-50% each day until 20mg is reached and then complete the programme as above. However it must be recognised that these large early reductions will probably result in intense withdrawal symptoms.
If required, ‚holding‘ on a given dose on one or two occasions during the detox may increase the client’s sense of control and decrease their anxiety. Delays in the rate of reduction should usually be accompanied by an increase in psychological support.
Longer-term detoxification: decreasing doses over 1-6 months
1 month detoxification regime
From a starting dose of 40mg:
From a starting dose of 25mg:
4 month detoxification regime
Following initial stabilisation, and a period in which the client remains heroin free, the daily dose can be reduced by 5mg or 10mg every week or fortnight until 30mg is reached.
The rate of reduction in the daily dose is then reduced to 5mg every week or fortnight until 10-15mg is reached. At this point daily dose reductions can be reduced to 2 or 2.5mg every week or fortnight.
A typical 4 month regime using these principles from a starting dose of 45mg would be:
6 month detoxification regime
A 6 month detox regime using the same principles as the 1-5 month detox, from a start of 60mg might be:
Detoxification following exclusion from a methadone prescribing programme
Sometimes methadone prescriptions are stopped. The reasons for doing this are discussed in Section 10: Practical issues in methadone prescribing – Terminating treatment.
The client should be aware of exactly what the rate of detox will be before the prescription is terminated. Abrupt cessation of opiates is not fatal in people who are otherwise healthy. The rate of reduction therefore usually seeks to strike a balance between continuance of the prescribing programme under a new guise, and a rate of reduction which gives the individual little chance of achieving abstinence if they want to.
A regime such as the following is commonly used:
and then:
However any of the above regimes could be employed.
Anxiety
Client expectations of anxiety are one of the best indicators of the intensity of withdrawal symptoms and there can be little doubt that the two are closely linked.
As with all anxiety-provoking situations, levels of anxiety during and after methadone detoxification can be reduced through information being given to the client about what they can expect to happen and why it is happening, and the opportunity being given to discuss the issues that are raised.
Emotions such as anger and depression can trigger withdrawal symptoms in people who are stabilised on methadone – this is known as ‚pseudo withdrawal syndrome‘. If clients become more aware of these feelings during a detox then this too will increase the severity of their withdrawal symptoms. Counselling during and after the detox can help deal with these emotions and reduce the physical consequences.
Abstinence phobia
S M Hall in 1979 described abstinence phobia as an exaggerated response to comparatively mild withdrawal symptoms.90
Indeed many clients become very anxious as soon as dose reductions begin and feel unable to continue with the detoxification. Hall suggested that previous actual or observed traumatic experience of withdrawal symptoms may be the cause of this fear. Unfortunately her attempts to use standard cognitive behavioural therapy in a controlled trial – which has been shown to be effective in other anxiety disorders – were unsuccessful.
This being the case, choices for clients who demonstrate high levels of anxiety during detox are limited as they are unlikely to achieve abstinence without considerable support. Slowing the rate of reduction and increasing support is the first line response. Following this in-patient detoxification or residential rehabilitation might be options.
If the anxiety cannot be resolved, and relapse is the outcome of all attempts at detox, the most appropriate response may be methadone maintenance.
Alternatives to methadone in detoxification
Clonidine
This is similar in its action to lofexidine (see below), the major difference being its more powerful hypotensive action which contra-indicates its use in anything other than an in-patient setting. Clonidine has never had a product licence for opiate detoxification.
Lofexidine (BritLofex)
Lofexidine hydrochloride is now fully licensed in the UK for management of the symptoms caused by withdrawal. Lofexidine is not an opiate and does not stimulate opiate receptors and therefore does not have the psychoactive effect nor the dependency potential of opiates.
It works by inhibiting the release of noradrenaline. Noradrenaline is a key chemical transmitter that acts on the nervous system, the action of which has been suppressed by opiates: see Section 4: The physiology and pharmacology of methadone.
As lofexidine is not an opiate, increasing the dose too quickly, or beyond the recommended maximum, will not necessarily reduce withdrawal symptoms but it will increase the risk of side effects such as hypotension (low blood pressure). This should be made very clear to patients who are self administering their lofexidine tablets.
The safety of lofexidine in pregnancy has not yet been established.
Lofexidine is unlikely to:
The effect of these factors can be reduced by:
Side effects
Hypotension (low blood pressure) is the principle possible side effect that can occur during treatment with lofexidine. Although this could prohibit its use for some clients and may result in discontinuation of treatment in others, in practice there is rarely a clinically significant reduction in blood pressure.
Blood pressure should be monitored, especially while the dose is increasing. For in-patients if the standing systolic BP has dropped by more than 30 mmHg (and is associated with symptoms of dizziness and light-headedness or over-sedation) the next dose of lofexidine should be withheld until the systolic BP is less than 30mmHg below the baseline.
Sedation is more likely to occur in clients concurrently prescribed (or taking) benzodiazepines and/or other central nervous system depressants.
Lofexidine is safe for community use in patients who are:
A typical 10 day out-patient lofexidine regime
Reduce the methadone dose to 15mg daily and ask the patient to take their last dose in the evening.
The following morning (detox day 1) begin the following regime:
| Day of detox | Maximum number of tablets to be taken in the morning | Maximum number of tablets to be taken at lunch time | Maximum number of tablets to be taken at 6pm | Maximum number of tablets to be taken at night |
|---|---|---|---|---|
| Day 1 | 2 | 0 | 0 | 2 |
| Day 2 | 2 | 0 | 2 | 2 |
| Day 3 | 2 | 2 | 2 | 2 |
| Day 4 | 3 | 2 | 2 | 3 |
| Day 5 | 3 | 3 | 3 | 3 |
| Day 6 | 3 | 1 | 2 | 3 |
| Day 7 | 2 | 0 | 2 | 3 |
| Day 8 | 2 | 0 | 1 | 2 |
| Day 9 | 1 | 0 | 0 | 1 |
| Day 10 | 0 | 0 | 0 | 1 |
Notes:
The patient must be told:
Dihydrocodeine
In an attempt to reduce the severity of withdrawal symptoms some services switch detoxifying clients from methadone to dihydrocodeine for the final part of the process – usually when the daily methadone dose reaches around 15mg.
The rationale for this is that dihydrocodeine is:
There have been no controlled trials comparing subjective experience of withdrawals when detoxing on methadone, heroin or dihydrocodeine, but some clinicians have found the switch helpful, particularly if the anxiety of withdrawal is focused on the problems of coming off methadone.
However the treatment can have drawbacks. The experience of a ‚high‘ on dihydrocodeine can be greater than with methadone and thus clients can attempt unsustainable methadone dose reductions in pursuit of the ‚reward‘ of a ‚better drug‘.
Switching drug can also detract from the other psychological causes of withdrawal symptoms, neglect of which is unlikely to be therapeutic.
The product licence for dihydrocodeine does not include treatment of opiate dependence.
Methadone v heroin in detoxification
There is a commonly held belief amongst drug users that the withdrawal symptoms are worse and more prolonged when coming off methadone than heroin.
Given that methadone is a longer-acting drug this is probably true. However the experience of withdrawal is probably exacerbated by factors which are different with regard to most methadone detoxes as opposed to most illicit heroin detoxes.
Most illicit heroin withdrawal symptoms are:
Most methadone withdrawal symptoms are:
These factors probably all increase the stress associated with methadone dose reductions and serve to increase the subjective experience of withdrawal symptoms. Discussion of these issues with the client will probably serve to reduce the severity of the withdrawal experience.
Follow up/relapse prevention
People who have been using opiates for some time and who detoxify using methadone often benefit from support and assistance for some time afterwards. Plans and support mechanisms for the period after the detox should be in place before it commences.
Risk of relapse is always high as there are many potential causes of relapse including:
The person who has succeeded in getting off opiates will need help to resist these cues to relapse. Often clients are reluctant to return to prescribing services for follow-up support and there are often few services for those that do.
Support that would help and could be provided by drug services includes:
Support that could be suggested/facilitated by drug services includes:
A wonderful Source: http://www.drugtext.org/library/books/methadone/section9.html#methtop
(lsw) Künstliches Heroin auf Rezept ist für viele Schwerstabhängige der letzte Weg aus dem Sumpf. Doch wann es eine flächendeckende Versorgung gibt, ist unklarer denn je. Nicht selten fehlt es einfach an Patienten mit den notwendigen Voraussetzungen.
Bund und Land sind mittlerweile willig, die Krankenkassen signalisieren Einverständnis – und doch läuft die Diamorphin-Abgabe für Schwerstabhängige in Baden-Württemberg nur schleppend an. Das unternehmerische Risiko, das eine neue Abgabestelle für künstliches Heroin birgt, ist oft zu groß. Nach Angaben des Gesundheitsministeriums steht die Stadt Stuttgart in den Startlöchern. Der Gemeinderat hat sich Ende November berichten lassen, wie die gesetzlichen Voraussetzungen für eine Abgabestelle sind. Doch: „Vor 2012 wird es sicher nichts“, schätzt Hans Gros, Suchthilfeplaner der Landeshauptstadt.
Bevor der Gemeinderat grünes Licht geben könne, müsse die Finanzierung stehen. Und danach dauere es sicher noch ein Jahr. Dabei würde Suchtmediziner Andreas Zsolnai, der die Anlaufstelle betreiben soll, am liebsten bald loslegen. Die rechtlichen Vorgaben seien erfüllt, auch Kooperationspartner habe er schon. „Doch wegen der Auflagen und des hohen Personalschlüssels ist das betriebswirtschaftliche Risiko so hoch, dass ein einzelner Arzt wie ich das nicht schultern kann.“
Bis sich die Abgabestelle trägt, braucht es nach Schätzung der Fachleute rund 50 Patienten. Sie müssen unter anderem mindestens 23 Jahre alt und seit fünf Jahren abhängig sein. Voraussetzung sind zudem zwei gescheiterte Therapieversuche, etwa mit Methadon. Die hohen Hürden führen dazu, dass laut Gesundheitsministerium von den rund 9000 Schwerstabhängigen im Land nur etwa 200 bis 300 die Voraussetzungen für die Diamorphin-Behandlung erfüllen.
Eine Anlaufstelle in Stuttgart könne sich durchaus tragen, sagt Zsolnai. Wie lange es aber dauere, bis die notwendigen Patienten auch in die Praxis kommen, könne er nicht schätzen. „Irgendjemand müsste für die Anfangszeit grade stehen. Es bräuchte vielleicht ein fünfjähriges Modellprojekt.“ Für die Räume gibt es ebenfalls enge Vorgaben – aus Sicherheitsgründen. Zsolnais derzeitige Praxis im Gesundheitsamt wäre zu klein. In seinen Augen drängt die Zeit, weil jederzeit Kooperationspartner abspringen könnten. „Wenn es nicht innerhalb des nächsten Jahres festgezurrt wird, besteht die Gefahr, dass es im Sande verläuft.“
Als mögliche Standorte für die Diamorphin-Zentren waren im Sommer auch noch Mannheim, Freiburg, Heilbronn, Tübingen, Singen, Ulm und Ravensburg im Spiel. Doch sieht es vielerorts nicht rosig aus. „Viele dieser Anlaufstellen werden sich wohl nicht realisieren lassen“, sagt Joachim Holzapfel, Leiter des Suchthilfezentrums in Karlsruhe. Meist fehlten Patienten.
quelle: http://www.mainpost.de/regional/main-tauber/Kuenstliches-Heroin-auf-Rezept;art21526,5904860
Hundreds of drug users from Iran are turning up in Afghanistan’s western Nimroz province, with some claiming they were dumped there as undesirables by police from their own country.
Afghan officials worry that Tehran is exporting its social problems, although Iranian diplomats say there is no such policy. Others say that at least some drug users congregate in Afghanistan because narcotics are so freely available there and there are none of the draconian punishments meted out by the Iranian authorities.
Reza, 27, told how he was detained as a drug user in his home city of Zahedan in Iran’s Sistan-Baluchestan province, and was then included among a group of Afghan refugees who were being deported.
“I have documents showing I’m an Iranian national,” he told IWPR. “When I apply to government offices in Nimroz, they tell me to go to the border and ask the Iranian frontier officers to let me cross over. But when I go there, Iranian border officials abuse me and refuse to let me enter my own country.”
Reza says he sleeps in religious shrines in Zaranj, the main provincial town in Nimroz, and survives on the food he gathers from rubbish piles. He recently helped bury a friend. aged 40 and like him from Zahedan, who he says died “for lack of drugs”.
“Other addicts buried him between two graves,” he said.
Another man, Hossein, 38, said he was detained after family members in Iran’s Zabol province went to the police to complain about his chronic addiction problem.
He too said he was packed off across the border as part of a group of deported Afghan nationals. When he showed Afghan police his Iranian ID, they made efforts to send him home, but guards on the other side of the border would not admit him.
Mohammad Anwar Muradi, the head of the provincial counter-narcotics department, said ten to 15 Iranian drug users were entering Nimroz every week.
“There are currently about 2,000 drug addicts in Nimroz province, 80 per cent of them Afghans and Iranians deported from Iran,” he said. “It isn’t yet clear why Iranian border officials are deporting their own nationals to Afghanistan.”
The provincial police chief Hajji Musa Rasuli says his men have detained around 40 Iranian nationals in the region in the past two months, but have yet to pinpoint those living in Zaranj. His officers have tried to send ten drug users back home in recent weeks but Iranian frontier guards would not let them in.
Hajji Najibullah Alami, chief of staff in the provincial governor’s office, said the matter had been raised with Iranian officials, but no satisfactory response had been received.
An Iranian diplomat at the consulate in Herat, speaking on condition of anonymity, flatly denied that his country was expelling its own citizens. He suggested that individuals claiming to be Iranian nationals were in fact Afghans who had been properly deported, and were now seeking a way back into Iran.
“Anyone who has documents can enter Iran and will be assisted by Iranian border officers,” he said.
Residents of Nimroz province say many Iranians come and go voluntarily to enjoy the free market in heroin and other drugs.
“There’s no rigorous control in border areas, so Iranians come over from the other side, buy drugs and go back,” restaurant owner Hajji Sultan said.
He went on to voice a belief that appears to be widespread and was even articulated by some of the officials interviewed for this article, “Iran is deliberately deporting its addicts to Afghanistan in order to spread lethal diseases among Afghans.”
The Afghan government is struggling to provide drug treatment centres for the expanding number of users, and health officials in Nimroz say they do not have the resources to admit Iranian nationals as well. The country’s counter-narcotics minister, Zarar Ahmad Moqbel, recently said there was capacity to treat just one per cent of the estimated one million addicts.
Dr Nur Ahmad, the provincial health chief for Nimroz province, said no clinics existed to run medical checks on individuals – whether returning Afghan refugees or Iranians – as they entered the country.
“Initial assessments indicate that 50 per cent of addicts in Nimroz province are using needles, which increases the incidence of diseases like HIV/AIDS and hepatitis,” he said.
Zia Ahmadi is an IWPR-trained journalist reporting from western Afghanistan.
Source: http://iwpr.net/report-news/iranian-drug-users-%E2%80%9Cdumped%E2%80%9D-afghanistan
Wer vom Rauschgift loskommen will, braucht einen Ersatzstoff. Ist der nicht zu bekommen, droht ein Rückfall in die Sucht.
von Henning Bielefeld
Nordenham – Die Drogenberatungsstelle Rose 12 ist in großer Sorge: Die Heroin-Abhängigen bekommen in der Wesermarsch kein Methadon oder andere Ersatzstoffe für das Rauschgift mehr. „Das ist für die betroffenen Menschen eine Katastrophe“, sagt die Mitarbeiterin Dörte Horstmann.
Weniger Kriminalität
Aber auch für die Bürger, die mit Rauschgift nichts zu tun haben, ist das eine schlechte Nachricht, betont sie. Denn Süchtige, die von einem Arzt legal mit Ersatzstoffen versorgt werden, müssen nicht mehr illegal Drogen kaufen, verüben keine Beschaffungskriminalität mehr, sind deutlich gesünder als Rauschgift-Konsumenten und können sogar einer geregelten Arbeit nachgehen und damit ihr eigenes Geld verdienen. Sie sind auf dem Weg zur Drogenfreiheit.
Deshalb fordern Dörte Horstmann und der Einrichtungsleiter von Rose 12 in Oldenburg, Winfried Wigbers, dass dieses Problem so schnell wie möglich gelöst wird. Vor gut einem Jahr gab es noch zwei niedergelassene Ärzte in der Wesermarsch, die Ersatzstoffe für Heroin – und nur um dieses Rauschgift geht es – nach strengstens festgelegten Kriterien ausgeben durften. Dem einen Arzt wurde diese Erlaubnis entzogen. Beim zweiten Arzt – er praktiziert in Brake – steht die Erlaubnis auf der Kippe, weil die Staatsanwaltschaft in dieser Angelegenheit gegen ihn ermittelt.
So lange diese Ermittlungen nicht abgeschlossen sind, könnte er theoretisch weiter Ersatzstoffe abgeben, sagt Winfried Wigbers. Aber der Mediziner sei auf unabsehbare Zeit krankgeschrieben und stehe nicht zur Verfügung. Da seine Praxis aber weiterhin bestehe, sehe die kassenärztliche Vereinigung keinen Grund, einen anderen niedergelassenen Arzt mit dem Substitutionsprogramm zu betrauen.
Deshalb müssen die Betroffenen auf unabsehbare Zeit nach Bremerhaven, Varel oder Oldenburg ausweichen, was vor allem für die Patienten schwierig ist, die einer regelmäßigen Arbeit nachgehen, aber kein Auto haben. Wer aber nicht rechtzeitig an den Ersatzstoff kommt, spürt Entzugserscheinen. Sie sind mit heftigen körperlichen Leiden verbunden, die an eine echte Grippe erinnern, erläutert Winfried Wigbers: Die Knochen tun weh, Übelkeit und Durchfall stellen sich ein. Die Betroffenen beginnen, sich ständig zu kratzen. In der Rauschgift-Szene wird dieser Zustand deshalb als „affig“ bezeichnet. Er treibt die Patienten in so große Not, dass sie nicht davor zurückschrecken, sich wieder Heroin zu beschaffen – und der Teufelskreislauf beginnt von neuem.
Die Situation ist auch deshalb gefährlich, weil es nicht leicht ist, einen niedergelassenen Arzt für die Teilnahme am Substitutionsprogramm zu gewinnen. Denn die Vorschriften sind äußerst streng, und wer sie missachtet, bekommt es mit dem Staatsanwalt zu tun. „Ärzte wollen vor allem ihren Patienten helfen“, erläutert Winfried Wigbers. Das können sie beispielsweise, indem sie dem Betroffenen Ersatzstoffe mit nach Hause geben, wenn sein Anfahrtsweg weit und er an einen Arbeitsplatz gebunden ist. Die Abgabe dieser „Take-Home“-Stoffe ist aber sehr streng reglementiert, so dass ein Arzt schnell in die Zwickmühle kommt, ob er seinem Patienten einen Ersatzstoff mitgibt oder sich an die Vorschriften hält und riskiert, dass der Patient Heroin kauft.
Viele Heroin-Abhängige
In der Wesermarsch ist die Lage auch deshalb brenzlig, weil es hier überdurchschnittlich viele Heroin-Abhängige gibt. Allein in Nordenham sind es 80 bis 90 – von ihnen nimmt jeder Zweite am Ersatzstoff-Programm teil –, ein weiterer Schwerpunkt ist Elsfleth. Warum ist das so? Winfried Wigbers zuckt die Schultern: „Oft liegt es an bestimmten Menschen. Ein Wortführer in einer Clique nimmt Heroin – und die anderen tun es ihm nach.“
ScienceDaily (Sep. 11, 2010) — Addictive drugs are known to induce changes in the brain’s reward circuits that may underlie drug craving and relapse after long periods of abstinence. Now, new research in the September 9 issue of the journal Neuron, uncovers a specific neural mechanism that may be linked to persistent drug-seeking behavior and could help to guide strategies for development of new therapies for cocaine addiction.
Previous research has shown that the ventral tegmental area (VTA) is a brain region that is activated when cocaine users experience a craving for cocaine after being exposed to cocaine-associated cues. The medial prefrontal cortex (mPFC), which receives input from the VTA via circuits that use the „reward“ neurotransmitter dopamine, has also been implicated in drug craving after cocaine withdrawal. Further, increases in the level of brain-derived neurotrophic factor (BDNF) have been observed in the VTA and mPFC in rats after withdrawal from repeated cocaine exposure.
„BDNF plays a key role in modulating the structure and function of synapses, the sites of communication between neurons. Therefore, increased BDNF after cocaine withdrawal may drive synaptic changes that contribute to compulsive drug seeking behavior,“ explains senior author, Dr. Mu-ming Poo from the University of California, Berkeley. „It has been shown that increased BDNF in the VTA after cocaine withdrawal in rats promotes the drug-dependent motivational state. However, nothing is known about the potential BDNF effect on synaptic function and plasticity in mPFC neurons after cocaine withdrawal.“
Dr. Poo and colleagues designed a study to examine how BDNF and the mPFC might contribute to relapse after cocaine addiction. The researchers found that the gradual increase in BDNF expression in the rat mPFC after terminating repeated cocaine exposure significantly enhanced the activity-induced potentiation of specific synapses. Dr. Poo’s group went on to uncover the specific cellular mechanism linking increased BDNF with enhanced synaptic plasticity and demonstrated that interference with the key molecule in the BDNF signaling process reduced behavioral sensitivity after cocaine withdrawal in rats.
„In short, our results demonstrate that elevated BDNF expression after cocaine withdrawal sensitizes the excitatory synapses in the mPFC to undergo activity-induced persistent potentiation that may contribute to cue-induced drug cravings and drug-seeking behavior,“ concludes Dr. Poo. Although a clear correlation between rat and human behaviors of cocaine craving and relapse remains to be established, the cellular mechanism uncovered in this study does appear to have behavioral relevance and may represent a direct brain sensitization that is involved in triggering relapse.
The researchers include Hui Lu, Pei-lin Cheng, Byung Kook Lim, Nina Khoshnevisrad, and Mu-ming Poo, University of California, Berkeley, Berkeley, CA.
source is:http://www.sciencedaily.com/releases/2010/09/100908121913.htm
You can download the Study here:TD_M1_Cocaine_and_BDNF
Erasing‘ drug-associated memories may prevent recovering drug abusers from relapsing, researchers at the University of Cambridge have discovered.
The team, led by Professor Barry Everitt, was able to reduce drug-seeking behaviours in rats by blocking a brain chemical receptor important to learning and memory during the recall of drug-associated memories. Their research, which was funded by the Medical Research Council, was reported in the 13 August issue of The Journal of Neuroscience.
The Cambridge scientists found that by disrupting or erasing memories associated with drug use during recall, they could prevent the memories from triggering relapses and drug taking.
Memories exist in different states depending on whether they are being recalled or not. When memories are recalled, they become ‚unstable‘ or malleable and can be altered or erased during the process called reconsolidation. Because relapse by drug abusers is often prompted when they recall drug-associated memories, the scientists found that by blocking these memories they could prevent relapse.
In order to undertake the experiments, the researchers trained rats to associate the switching on of a light with cocaine. The researchers then exposed the rats to the light, thereby ‚reactivating‘ the memory, without the cocaine. In an effort to receive more cocaine, the rats would perform tasks that the scientists had created which would turn on the light.
When the animals were given a chemical that interfered with the action of the NMDA-type glutamate receptor (which plays an important role in memory) prior to the ‚reactivation‘ session, the rats showed reduced cocaine-seeking behaviours. A single treatment reduced or even stopped drug-seeking behaviours for up to four weeks.
In contrast, blocking the receptors after or without the reactivation session had no effect on subsequent drug-seeking behaviours, indicating that drug-associated memories can be disrupted during but not after reconsolidation of memories.
Professor Barry Everitt said, „The results suggest that efforts should be made to develop drugs that could be given in a controlled clinical or treatment environment in which addicts would have their most potent drug memories reactivated. Such treatments would be expected to diminish the effects of those memories in the future and help individuals resist relapse and maintain their abstinence.“
Dr Amy Milton, a co-author, said, „This is a new approach to the treatment of drug addiction that has great potential. Additionally, this might also be used to treat other neuropsychiatric disorders characterized by maladaptive memories, including post-traumatic stress and phobic anxiety disorders.“
Source: http://www.sciencedaily.com/releases/2008/08/080812213931.htm
I started seeing Daniel in June 2005 at a small urgent-care clinic I run for mostly injection-drug users on skid row. An addict, he was a tall, thin man with long, stringy gray hair and an unkempt beard. My notes from our initial conversation described him as „disheveled, dirty and lethargic.“ On subsequent visits, he often had food or vomit in his beard and would come to the clinic smelling of urine. He seldom had much to say.
Then, in May 2006, I saw a different side of Daniel, whom I will refer to only by his first name to protect his privacy, although he has agreed to let me tell his story. During one of his visits to the clinic, he kept his head down and tears welled up in his powder-blue eyes, but he talked as he never had before. Things weren’t good. He’d been jumped the previous week, he told me in his Kentucky drawl. He hated who he’d become, he said — a loner, someone who didn’t care about others. „I used to play the guitar professionally,“ he said regretfully. „I was in a band. I had a life.“
Listening to him, I had a realization: He was severely depressed. Until then, I’d assumed that he, like so many others on skid row, was schizophrenic. Schizophrenia is frustratingly difficult to treat, but depression has many effective treatments. My realization about his depression also put his addiction in a different light. He might well be using heroin in an attempt to treat his depression.
Most of the drug addicts I see are self-treating, whether for mental illness, chronic pain or both. Perhaps if we could treat the underlying depression, Daniel might be able to stop self-medicating with heroin. Homeless people die young: Their average lifespan, according to studies, is 47. So getting Daniel off drugs and off the streets was a high priority.
That did not prove easy. I tried, after realizing he was depressed, to refer him to a mental health clinic. But he never went. Finally, I gave him some samples of Seroquel, which treats depression and psychosis. After that, I didn’t see him for two months. When he finally came again, he had a short explanation: „Got picked up.“ Jail. „I was thinking about ending it all, Doc…. on my birthday.“ Again I prodded him to try the Seroquel.
Instead, he again quit coming to the clinic regularly.
Through much of 2007 and 2008, I saw Daniel only sporadically. He came in when he had a medical issue that needed attention — at one point he had a painful groin hernia — then we didn’t see him for a while. But there was one big change in 2008. A new county program was connecting mentally ill homeless patients with case managers who could help them obtain psychiatric and medical care, drug treatment and housing.
Daniel qualified for the program and was assigned to a caseworker, Pearlina. But I soon heard that he wasn’t keeping his appointments with her. Meanwhile, he had increased his heroin use to deal with the pain from his hernia. Because of his addiction, finding a hospital that would perform surgery was complicated.
I called his caseworker. „Pearlina,“ I told her, „you’re going to have to come to the needle exchange in order to see him.“ She agreed, and the director of the needle exchange agreed to call the next time Daniel showed up.
Finally, Daniel met with Pearlina at the needle exchange. But he continued to frustrate us. He never kept the psychiatry appointments I made for him. And he also missed a preoperative appointment to get his hernia taken care of. Pearlina found a sober-living home for Daniel, but he left after a day.
Over the next couple of months, there were a few signs of progress, but they were usually followed by disappointment. James took Daniel to the Department of Motor Vehicles to get an ID card. He also hooked him up with a methadone clinic. But then Daniel missed his appointment with the methadone clinic because he got arrested.
In December 2008, looking at Daniel’s now mango-sized hernia, I realized we needed to intervene more dramatically. He couldn’t stop heroin because of the pain from his hernia. He couldn’t get clean without being housed. Finally, the Harbor- UCLA family medicine team agreed to hospitalize Daniel for his pre-op evaluation, and a surgeon colleague agreed to operate on him. Pearlina found Daniel housing at the Weingart Center in the skid row area, so he would have a place to go after discharge. I requested that Daniel be provided with methadone while he was hospitalized. And James got a methadone clinic to hold a spot for Daniel for when he was discharged. Most important, Daniel agreed to it all.
On Feb. 9, 2009, Daniel had surgery. The next month, at his request, he entered a detox program, followed by a 90-day residential drug treatment program. He also started taking psychiatric medication.
When I next saw him, a couple of months later, his hair was shiny and his beard was nicely trimmed. He had gained about 40 pounds. He had life in his powder-blue eyes.
Studies have shown that housing the homeless cuts death rates by up to 500%, and that assertive community treatment for people with mental illness, which includes housing, results in people being 62% less symptomatic. These things often take, as was the case with Daniel, a team of professionals all pulling in the same direction. That kind of intervention and care are expensive. But in many cases, they are far less expensive than the alternative: a cycle of arrests, hospitalizations and emergency medical treatments.
Despite their effectiveness, county programs like the one that helped Daniel are always threatened by budget constraints. But we need to keep fighting for them, so that men and women like Daniel have a shot at fulfilling lives.
After Daniel’s drug treatment, Pearlina and others helped him find a sober-living house in San Pedro. He’s still there today, where he remains clean and sober. He’s saving up to buy a guitar.
Susan Partovi is an attending physician at Harbor-UCLA and the medical director for Homeless Health Care Los Angeles.
Four Cases Involving Extraction of Fentanyl From
Transdermal Patches
Amy M. Tharp, MD, Ruth E. Winecker, PhD, and David C. Winston, MD, PhD
Abstract: The transdermal fentanyl system delivers a specific dose
at a constant rate. Even after the prescribed application time has
elapsed, enough fentanyl remains within a patch to provide a
potentially lethal dose. Death due to the intravenous injection of
fentanyl extracted from transdermal patches has not been previously
reported. We present 4 cases in which the source of fentanyl was
transdermal patches and was injected. In all of these cases, the
victim was a white male who died at home. Case 1 was a 35-year-old
with no known history of drug use, who was found by his wife on
the floor of his workshop. Police recovered a fentanyl patch, needle,
and syringe at the scene. Case 2 was a 38-year-old with a known
history of drug use whose family claimed that he was in a treatment
program that used fentanyl patches for unknown reasons. His
brother found him dead in bed, and law enforcement officers found
a hypodermic needle beside the body; a ligature around his left hand,
and apparent needle marks between his first and second digits were
also noted. Case 3 was a 42-year-old with a recent attempted suicide
via overdose who was found dead at his home. An empty box of
fentanyl patches, Valium, Ritalin, and 2 syringes were found at the
scene. Case 4 was a 39-year-old found by his mother, who admitted
to removing a needle with attached syringe from the decedent’s arm.
Medications at the scene included hydrocodone, alprazolam, zolpidem,
and fentanyl patches. All reported deaths were attributed to
fentanyl intoxication, with blood concentrations ranging from 5 to
27 g/L.
From the Department of Pathology, Wake Forest University School of
Medicine, Winston-Salem, North Carolina (A.M.T.); Office of the Chief
Medical Examiner, Chapel Hill, North Carolina (R.E.W.); Forensic
Science Center, Tucson, Arizona (D.C.W.); and Department of Pathology,
University of Arizona College of Medicine (D.C.W.).
entanyl overdose is classically associated with intravenous
use of -methyl-fentanyl (“China White”),1 a powder
form that is chemically different from therapeutic fentanyl.
However, fentanyl overdose has also been reported in
cases of excessive transdermal application2 and ingestion3,4
or inhalation5 of transdermal patches. Fentanyl is a narcotic
analgesic, which primarily binds to opioid -receptors, producing
not only the analgesia for which it is primarily used
but also sedation, euphoria, and at high doses, respiratory
depression and death.6 Transdermal fentanyl therapy (Duragesic;
Janssen Pharmaceutica, Beerse, Belgium) has been used
successfully to treat postoperative pain, as well as pain
associated with malignancies, but as with all opioid agents,
the potential for abuse exists. The transdermal fentanyl system
is designed to deliver a specific dose at a constant rate
based on the initial concentration present in the patch. This
delivery system effectively limits the peak versus trough
concentration, which is a common problem associated with
other routes of administration. Following 3 days of continuous
therapeutic use, enough fentanyl remains within a patch
to provide a potentially lethal dose.7 We present 4 cases
occurring in North Carolina between January 1997 and July
2001 in which the fatal dose of fentanyl was extracted from
transdermal patches and injected intravenously.
MATERIALS AND METHODS
Case Selection
The case files of the Office of the Chief Medical
Examiner (Chapel Hill, NC) were searched from 1991 to
2001 for deaths related to fentanyl. An initial search identified
53 cases,8 of which only 4 involved intravenous abuse of
a transdermal fentanyl patch. Case histories are listed below.
Toxicologic Analysis
All toxicologic analyses were performed at the Office
of the Chief Medical Examiner (Chapel Hill, NC). All cases
were screened for volatiles, common drugs of abuse (eg,
cocaine and morphine), and other basic drugs. Other tests (eg,
fentanyl) were performed as needed.
Fentanyl Screen
The specimens were screened by enzyme linked immunoassay,
with a 1 g/L cutoff concentration (Orasure Technologies,
Bethlehem, PA) utilizing a Biochem Personal Laboratory
Autoanalyzer (Allentown, PA). The assays were performed in
accordance with the manufacturers instructions and as validated
for use in the Office of the Chief Medical Examiner Toxicology
Laboratory.9
Fentanyl Confirmation and Quantification
Quantification and confirmation analyses were performed
by first isolating fentanyl by basic extraction6 of a 1to
5-mL (g) specimen. Underivatized specimens were analyzed
on an Agilent Technologies (Wilmington, DE) gas
chromatograph/mass spectrometer (GC/MS). The GC/MS
system was composed of an Agilent 6890 gas chromatograph,
a 5973 mass selective detector (MSD) and a 7683 liquid
auto-sampler. The GC/MS was fitted with a HP-1MS capillary
column (30 m .
0.25 mm inside diameter .
0.25-m
film thickness). A 13.19-minute run time occurred after 1-L
splitless injection into a 275°C injection port equipped with
0.4-mm gooseneck liner with base-deactivated fused silica
wool. Oven temperature programming began at 125°C, holding
for 1.00 minute, then ramping at 3 intervals: 35°C/minute
to 195°C, 7°C/minute to 230°C and 32°C/minute to a final
temperature of 300°C, holding for 3 minutes. Helium was
used as the carrier gas at a linear velocity 61 cm/s; flows
included a septum purge of 15.0 mL/minute at 2.0 minutes
and a constant column flow of 2.6 mL/minute. The MSD was
operated in selective ion mode, with a transfer line temperature
of 280°C.
CASE PRESENTATIONS
Case 1
A 35-year-old Caucasian man with no known history of
drug use was working in his workshop at home one evening.
His wife reported that at approximately 12:30 AM, she asked
him to come into the house, but that he stated that he would
probably continue building porch swings through the night.
His father, who stated that he “appeared OK,” last saw him
alive at 2:30 AM. At approximately 5:00 AM, the decedent’s
wife found him lying on the floor of his workshop. Paramedics
were unable to resuscitate him. Police investigating the
scene found a fentanyl patch, a needle, and syringe in the
workshop. External examination of the body revealed no
evidence of trauma, except for a 3/4-inch recent contusion
with some yellow discoloration at its margins in the left
antecubital fossa and a faint petechial-like contusion along a
vein on the right forearm. Pulmonary congestion and edema,
with a combined lung weight of 920 g, were the only other
significant autopsy findings. Toxicological analysis of aortic
blood was remarkable for a fentanyl concentration of 5 g/L,
as well as a concentration of 0.8 mg/L of propoxyphene
(generally considered to be a nontoxic concentration), and
therapeutic concentrations of amitriptyline (0.08 mg/L) and
its metabolite nortriptyline (0.33 mg/L). No other organic
bases were detected, and testing for norpropoxyphene was
not performed. The cause of death was attributed to “fentanyl
poisoning,” with the manner of death listed as accident.
Case 2
A 38-year-old Caucasian man with a history of drug use
was living with his relatives. His family claimed that he had
begun a treatment of his drug use in a program that used
“morphine patches” for unknown therapeutic purposes. He
was last seen alive at 10:00 PM, at which time he complained
of nausea. His brother found him dead in bed the following
morning at 8:15 AM. Resuscitative efforts were attempted but
were unsuccessful. Law officers found a hypodermic needle
in the bed beside the body and a ligature on his left hand, with
apparent needle marks between the thumb and forefinger. On
external examination at the time of autopsy, scars were noted
in the right antecubital fossa as well as over each wrist,
including a relatively recent puncture site over the dorsum of
the left hand, between the thumb and second digit. Internal
examination revealed pulmonary congestion and edema, with
a combined lung weight of 1500 g, and cardiomegaly (450 g).
A focus of granulomatous inflammation was present within
the left lung with caseous necrosis, which was found to be
due to Coccidioides immitis on silver stains. Focal chronic
hepatitis and moderate coronary atherosclerosis were also
identified. Toxicologic studies of aortic blood were positive
fora27 g/L concentration of fentanyl, with no other
substances identified. The cause of death was listed as “fentanyl
poisoning” with the manner of death as accident.
Case 3
A 42-year-old Caucasian man was found dead in his
home, lying prone in the hallway, with his eyeglasses broken
and hanging from his face. He had last been known to be
alive on the previous day at 10:30 PM, when he had answered
a phone call. At the scene, a bottle of diazepam with 11 pills
missing from the prescribed number, a methylphenidate tablet,
and 2 syringes (1 empty and 1 filled with a clear liquid),
as well as an empty box of fentanyl patches were recovered.
He had a history of ethanol and multisubstance abuse and was
seen in his local emergency room the week prior to his death
for treatment of an attempted suicide by Percocet and Restoril
overdose, as well as self-inflicted abrasions and lacerations,
and ethanol intoxication. Following a work-up, gastric decontamination,
and observation, he was sent to a psychiatric
hospital for involuntary commitment. It was not determined
how he came to be at his home on the day of his death.
External examination was unremarkable, with the exception
of abundant healed apparently self-inflicted incised wounds
© 2004 Lippincott Williams & Wilkins
on the wrists, abdomen, and forearms. No fentanyl patches
were found on the body. Pulmonary congestion and edema,
with a combined lung weight of 1920 g, cardiomegaly (450
g), with mild coronary atherosclerosis, and mild hepatic
steatosis were found at autopsy. Aortic blood was sent for
toxicologic analyses and was positive for 17 g/L of fentanyl,
0.49 mg/L of paroxetine, low concentrations of cocaine
(0.061 mg/L) and its metabolite, benzoylecgonine (0.36 mg/
L), and diazepam (0.15 mg/L). Fentanyl overdose was listed
as the cause of death and the manner of death was classified
as suicide.
Case 4
A 39-year-old Caucasian man complained of a fever,
sore throat, and malaise. He was seen in his local urgent care
facility and given hydrocodone cough syrup. Two weeks
later, he was found unresponsive in the bathroom of his home
by his mother, who admitted removing a needle with attached
syringe from his arm. Also found at the scene were 2 empty
bottles of hydrocodone, a one-third full bottle of hydrocodone
syrup, empty bottles of alprazolam and zolpidem, 2 additional
syringes, and 2 empty wrappers from fentanyl patches. He
was taken to the local emergency room, where he was
pronounced dead. Further investigation revealed a history of
drug use, asthma, depression, and psychosis. At the time of
autopsy, old needle puncture sites were found within bilateral
antecubital fossae, with a relatively recent needle puncture in
the left antecubital fossa. Microscopic examination of these
sites revealed dermal foreign body giant cells with polarizable
material. Internal findings included cardiomegaly (510
g) with left ventricular hypertrophy and hepatosplenomegaly.
Numerous foreign body giant cells with polarizable material
were present within the lungs, surrounding the pulmonary
blood vessels. Toxicologic analysis of femoral blood was
positive for 13 g/L of fentanyl, 0.083 mg/L of hydrocodone,
and 0.076 mg/L of oxycodone. Testing of the syringe found
at the scene was positive for fentanyl. The cause of death was
determined to be fentanyl toxicity, with hydrocodone and
oxycodone listed as significant contributing factors. The manner
of death was determined to be accident.
DISCUSSION
Fentanyl, developed by Janssen Pharmaceutica, was
originally introduced in the United States in 1968 for use as
an intravenous analgesic-anesthetic drug. The abuse of fentanyl
has classically been by health care professionals who
had access to the controlled drug. In the 1980s, a street
version began to appear, resulting in many deaths. “China
White,” or -methyl-fentanyl, was found to be up to 1000
times more potent than heroin1 and with demographics similar
to those of heroin abuse.10 In particular, Caucasian men
with an average age of 32 years old and a prior history of
intravenous drug use were most likely to abuse China White
usually in combination with other drugs (alcohol, cocaine,
other opiates). The FDA approved Duragesic (Janssen Pharmaceutica,
Beerse, Belgium), the first transdermal fentanyl
system, in 1990 for use in the control of chronic and postsurgical
pain.
Since their introduction in 1990, transdermal fentanyl
patches have been abused in a number of ways. Edinboro et
al2 reported a case of an 83-year-old female with terminal
cancer who was found to have fatal levels of fentanyl in her
blood (25 g/L) after applying 3 patches to her chest. Arvanitis
and Satonik3 described a case of a 38-year-old man who
was found unresponsive on 3 separate occasions after chewing
transdermal fentanyl patches. He was treated successfully
with naloxone the first 2 times, but the final time, he was
found dead with a fentanyl patch in his oropharynx. Complete
postmortem evaluation and toxicologic analyses were not
complete at the time of publication. Another case of intentional
oral ingestion of fentanyl patches was reported by
Purucker and Swann,4 who described a 24-year-old woman
who reported to her local emergency room complaining of
pain due to miscarriage, as well as chronic pain and muscle
spasms. She received an intramuscular injection of meperidine
and a fentanyl patch was applied for continued pain
relief. She was found shortly thereafter in the lavatory,
unresponsive and apneic. She was successfully resuscitated,
and an empty Duragesic (Janssen Pharmaceutica) patch was
found in her wallet, with bite marks found on the polyester
backing and none of the fentanyl gel remaining in the patch.
Neither a urine drug screen nor serum fentanyl level was
obtained. Marquardt and Tharratt5 reported a case of a 36year-
old man who became apneic, hypotensive, and tachycardic
following heating of a fentanyl patch with subsequent
inhalation of the evolving vapors, which was witnessed by his
girlfriend. Naloxone was administered and he was able to be
resuscitated; urine or serum drug screens were not performed
at that time. This man subsequently died as a result of further
inhalation abuse of fentanyl patches, and (according to Marquardt
and Tharratt5) he was found at autopsy to have the
following fentanyl concentrations: femoral blood, 2.66 ng/
mL; urine, 41 ng/mL; and liver, 122 ng/mL.
Transdermal fentanyl therapy consists of a patch composed
of 4 layers with an outer protective liner. The 4 layers
include a polyester film backing; the drug reservoir, which
contains a mixture of fentanyl, alcohol, and hydroxyethyl
cellulose; a membrane that controls the rate of fentanyl
delivery; and a silicone adhesive, which also contains fentanyl.
The rate-limiting step in absorption is through the lipophilic,
keratinous stratum corneum by passive diffusion.11
Extraction of the contents of the drug reservoir followed by
intravenous injection of the fentanyl effectively bypasses this
rate-limiting step and provides a bolus dose. This unique
method of abuse, therefore, increases a person’s risk of fatal
overdose by rapidly administering larger than the usual in
© 2004 Lippincott Williams & Wilkins
The American Journal of Forensic Medicine and Pathology • Volume 25, Number 2, June 2004 Fatal Intravenous Fentanyl Abuse
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