Effects of Buprenorphine and Hepatitis C on Liver Enzymes in Adolescents and Young Adults

Dept. of Psychiatry, University of New Mexico School of Medicine, MSC09 5030, 1 University of New Mexico, Albuquerque, NM, 87131-0001, USA.
Journal of Addiction Medicine (Impact Factor: 1.76). 12/2010; 4(4):211-6. DOI: 10.1097/ADM.0b013e3181c4e27e
Source: PubMed


The purpose of this study was to explore changes in transaminase values associated with buprenorphine treatment and hepatitis C status among opioid dependent subjects aged 15-21.
152 subjects seeking treatment for opioid dependence were randomized to 2-week detoxification with buprenorphine/naloxone (DETOX) or 12 weeks buprenorphine/naloxone (BUP). Liver chemistries including transaminases were obtained baseline and at 4, 8, and 12 weeks. 111 patients had at least one set of transaminases during treatment and were included in analyses of treatment effects.
Overall, 8/60 BUP participants vs. 12/51 DETOX participants had at least one elevated ALT value during follow-up (Chi-square n.s.). 5/60 BUP participants vs. 11/51 DETOX participants had at least one elevated AST value (Chi-square = 3.194, p = .048). Twenty-eight out of 152 participants were hepatitis C (HCV) positive at baseline, and 4 seroconverted within 12 weeks, 2 in each group. HCV status was significantly associated with transaminase abnormalities (p = .009 and p = .006 for ALT an AST, respectively). HCV status had a strong effect on transaminase abnormalities among participants assigned to DETOX, but not among those assigned to BUP.
No evidence was found for hepatotoxicity of buprenorphine in this exploratory analysis. HCV was present in a significant minority of participants and was a significant predictor of transaminase elevation. Results suggest that stabilization on buprenorphine may decrease the frequency of transaminase abnormalities associated with HCV in opioid dependent young people. The high rate of seroconversion underscores the importance of effective treatment and prevention.

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Available from: Michael P Bogenschutz, Jul 27, 2014
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    • "Zusätzlich verschärft wird die Situation, wenn auch noch andere (Gift-)Stoffe abgebaut werden müssen, welche in vielen Fällen ebenfalls über diese Enzyme metabolisiert werden.Antonilli et al. 2005, Tolson et al. 2009de Araujo et al. 1997). In einer explorativen Untersuchung (n = 152, 18% HCV+) wurde keine Evidenz für eine Hepatoxizität von Buprenorphin gefunden (Bogenschutz et al. 2010). Andererseits wurde ein Fall beschrieben, der darauf schließen lässt, dass Buprenorphin bei anfälligen Personen auch in therapeutischen Dosen Leber-und Nierenversagen auslösen kann, möglicherweise durch direkte mitochondriale Toxizität (Zuin et al. 2009). "

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