Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Methadone versus buprenorphine in opioid-dependent HIV patients on antiretrovirals


Published on

Published in: Health & Medicine
  • Be the first to comment

  • Be the first to like this

Methadone versus buprenorphine in opioid-dependent HIV patients on antiretrovirals

  1. 1. Methadone versus buprenorphine in opioid-dependent HIV patients on antiretrovirals Copyright © by Lorena Tonarelli, M.Sc. 2014 The μ-opioid agonist methadone and the μ-opioid partial agonist buprenorphine are prescribed for treating opioid dependence in patients with immunodeficiency virus (HIV) infection. Adverse interactions have been reported between these opioids and HIV antiretroviral (ARV) agents, which may reduce treatment effectiveness and contribute to negative clinical outcomes. We report the results of clinical pharmacology studies comparing the pharmacokinetic interactions of currently available ARV agents with methadone and buprenorphine. Opioids and ARVs are metabolized by CYP450 enzymes, particularly CYP3A4. Antiretrovirals that induce CYP3A4 activity, including the protease inhibitors lopinavir/ritonavir (LPV/r) and the reverse-transcriptase inhibitors efavirenz (EFV) and zidovudine (AZT), decrease methadone exposure. Therefore, the simultaneous administration of any of these antiretrovirals and methadone is associated with opioid withdrawal, requiring an average methadone dose increase of 50%. Complications include toxicity, non-adherence with antiretroviral regimens and consequent development of viral resistance, and illicit drug use. Buprenorphine has nonsignificant pharmacodynamic interactions with R, EFV and AZT, and no interactions with LPV/r. Potentially clinically significant increases in buprenorphine concentrations occur with the protease inhibitors atazanavir/ ritonavir (ATV/r). Unlike methadone, buprenorphine is metabolized to a biologically active compound (norbuprenorphine) and has high affinity for μ-opioid receptors and long receptor half-life. This could explain the lack of significant interactions between buprenorphine and antiretrovirals. We conclude that, in patients with cooccurring HIV disease and opioid dependence, buprenorphine has fewer clinically significant interactions with antiretroviral agents than methadone. Dose adjustments of the μ-opioid partial agonist thus may not be necessary, and the risk for toxicities, lack of adherence to ARV treatment, and negative clinical outcomes is potentially reduced. 1