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 to 21 years.
One hundred fifty-two subjects seeking treatment for opioid dependence were randomized to 2-week detoxification with buprenorphine/naloxone (DETOX) or 12 weeks with buprenorphine/naloxone (BUP). Liver chemistries including transaminases were obtained baseline and at 4, 8, and 12 weeks. One hundred eleven patients had at least one set of transaminases during treatment and were included in analyses of treatment effects.
Overall, 8 of the 60 BUP participants versus 12 of the 51 DETOX participants had at least one elevated alanine aminotransferase value during follow-up (χ2 = ns). Five of the 60 BUP participants versus 11 of the 51 DETOX participants had at least one elevated aspartate aminotransferase value (χ2 = 3.194, P = 0.048). Twenty eight of the 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 = 0.009 and 0.006 for alanine aminotransferase and aspartate aminotransferase, 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.
From the Department of Psychiatry (MPB, PJA, RK), University of New Mexico School of Medicine, University of New Mexico, Albuquerque, NM; University of New Mexico Center on Alcoholism, Substance Abuse, and Addiction (MPB, RK, JST), Yale, SE, Albuquerque, NM; and Department of Psychiatry (GEW), University of Pennsylvania and Treatment Research Institute, Philadelphia, PA.
Received for publication August 17, 2009; accepted October 7, 2009.
Send correspondence and reprint requests to Michael P. Bogenschutz, University of New Mexico Center on Alcoholism, Substance Abuse, and Addiction, 2650 Yale, SE, Albuquerque, NM, 87106. e-mail: email@example.com
This study is based on data from the National Institute on Drug Abuse Clinical Trials Network Study CTN 0010 (Dr. Woody, PI). Supported by the following grants from the National Institute on Drug Abuse and the National Institute on Alcohol Abuse and Alcoholism: U10-DA15833 K24-AA016555 (to M.P.B.); U10-DA13043 and KO5-DA17009 (to G.E.W.); and K02AA000326 (to J.S.T.). Reckitt Benckiser provided medication for the study.