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M34 Use of Buprenoprhine in the Treatment of Opioid Addiction

Section 1: Introduction

  • Purpose of the manual: Clinical Guidelines for the Use of Buprenorphine in the Treatment of Opioid Addiction; consensus- and evidence-based guidance to help physicians use buprenorphine in treating opioid addiction.
  • Scope of topics: physiology and pharmacology of opioids; opioid addiction and buprenorphine treatment; screening and assessment; detailed treatment protocols; management of special populations; policies and procedures for office-based opioid addiction treatment under DATA 2000.
  • Opioid addiction context in the United States: includes heroin and prescription opioid misuse/abuse (hydrocodone, oxycodone, meperidine).
  • Trends and treatment capacity: prescription opioid misuse and ED visits rising; heroin addiction increasing; methadone maintenance reduces opioid use and related crime but OTP capacity lags behind demand.
  • Buprenorphine as a new option: FDA-approved forms Subutex® (buprenorphine) and Suboxone® (buprenorphine/naloxone) enabling office-based treatment under DATA 2000; DATA 2000 waivers expand access outside OTPs.
  • Historical context summary:
    • Methadone maintenance (1960s) validated but historically restricted to OTP settings; stigma and daily OTP visits limited access.
    • LAAM approved in 1990s but production and regulatory issues persisted.
    • DATA 2000 (2000) created waivers for physicians to treat opioid addiction with Schedule III–V medications in non-OTP settings.
    • Subutex® and Suboxone® approved in 2002 as first such agents for office-based treatment.
  • Practical framing: guidelines serve as a resource for initial screening, assessment, determining appropriateness for buprenorphine, implementing treatment protocols, addressing comorbidities, and navigating policy/consent/privacy issues.

Section 2: Pharmacology

  • General opioid pharmacology overview
    • Opioid receptors: mu, delta, kappa; mu receptor activation mediates analgesia, euphoria, and addictive effects.
    • Agonists vs antagonists vs partial agonists:
    • Full mu agonists: activate receptors fully (e.g., morphine, heroin, methadone).
    • Antagonists: block receptor activation (e.g., naloxone, naltrexone).
    • Partial agonists: activate receptors but with a ceiling effect; do not activate to the extent of full agonists (e.g., buprenorphine).
    • Repeated opioid agonist use leads to tolerance and physical dependence; withdrawal occurs with reduction/cessation.
  • Buprenorphine as a mu receptor partial agonist
    • High receptor affinity with low intrinsic activity; displaces full agonists from receptors.
    • Slow dissociation from mu receptors => long duration of action and less frequent dosing possible (e.g., daily or less often in some regimens).
    • Ceiling effect: at higher doses, additional receptor activation does not increase effect; contributes to safety (e.g., reduced risk of fatal respiratory depression in overdose).
    • Reinforcing effects at analgesic doses in