Hepatitis after intravenous buprenorphine misuse in heroin addicts

被引:52
作者
Berson, A [1 ]
Gervais, A
Cazals, D
Boyer, N
Durand, F
Bernuau, J
Marcellin, P
Degott, C
Valla, D
Pessayre, D
机构
[1] Hop Beaujon, INSERM, U481, F-92118 Clichy, France
[2] Hop Beaujon, Serv Hepatol, F-92118 Clichy, France
[3] Hop Beaujon, Lab Anatomopathol, F-92118 Clichy, France
关键词
buprenorphine; heroin; hepatitis; Mitochondria; steatosis;
D O I
10.1016/S0168-8278(00)00049-0
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background: Sublingual buprenorphine is used as a substitution drug in heroin addicts. Although buprenorphine inhibits mitochondrial function at high concentrations in experimental animals, these effects should not occur after therapeutic sublingual doses, which give very low plasma concentrations. Case reports: We report four cases of former heroin addicts infected with hepatitis C virus and placed on substitution therapy with buprenorphine. These patients exhibited a marked increase in serum alanine amino transferase (30-, 37-, 13- and 50-times the upper limit of normal, respectively) after injecting buprenorphine intravenously and three of them also became jaundiced. Interruption of buprenorphine injections was associated with prompt recovery, even though two of these patients continued buprenorphine by the sublingual route. A fifth patient carrying the hepatitis C and human immunodeficiency viruses, developed jaundice and asterixis with panlobular liver necrosis and microvesicular steatosis after using sublingual buprenorphine and small doses of paracetamol and aspirin, Conclusions: Although buprenorphine hepatitis is most uncommon even after intravenous misuse, addicts placed on buprenorphine substitution should be repeatedly warned not to use it intravenously, Higher drug concentrations could trigger hepatitis in a few intravenous users, possibly those whose mitochondrial function is already impaired by viral infections and other factors. (C) 2001 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved.
引用
收藏
页码:346 / 350
页数:5
相关论文
共 24 条
[1]   Mechanisms for experimental buprenorphine hepatotoxicity:: major role of mitochondrial dysfunction versus metabolic activation [J].
Berson, A ;
Fau, D ;
Fornacciari, R ;
Degove-Goddard, P ;
Sutton, A ;
Descatoire, V ;
Haouzi, D ;
Lettéron, P ;
Moreau, A ;
Feldmann, G ;
Pessayre, D .
JOURNAL OF HEPATOLOGY, 2001, 34 (02) :261-269
[2]   THE SYSTEMIC BIOAVAILABILITY OF BUPRENORPHINE BY VARIOUS ROUTES OF ADMINISTRATION [J].
BREWSTER, D ;
HUMPHREY, MJ ;
MCLEAVY, MA .
JOURNAL OF PHARMACY AND PHARMACOLOGY, 1981, 33 (08) :500-506
[3]  
DESCHAMPS D, 1991, J PHARMACOL EXP THER, V259, P894
[4]   HEPATIC MITOCHONDRIAL-DNA DELETION IN ALCOHOLICS - ASSOCIATION WITH MICROVESICULAR STEATOSIS [J].
FROMENTY, B ;
GRIMBERT, S ;
MANSOURI, A ;
BEAUGRAND, M ;
ERLINGER, S ;
ROTIG, A ;
PESSAYRE, D .
GASTROENTEROLOGY, 1995, 108 (01) :193-200
[5]   THE BIOCHEMICAL EFFECTS AND TOXICITY OF HYDRAZINE IN CULTURED RAT HEPATOCYTES [J].
GHATINEH, S ;
TIMBRELL, JA .
TOXICOLOGY IN VITRO, 1994, 8 (03) :393-399
[6]   BUPRENORPHINE - REVIEW OF ITS PHARMACOLOGICAL PROPERTIES AND THERAPEUTIC EFFICACY [J].
HEEL, RC ;
BROGDEN, RN ;
SPEIGHT, TM ;
AVERY, GS .
DRUGS, 1979, 17 (02) :81-110
[7]  
HIRSCHAUER C, 1989, GASTROEN CLIN BIOL, V13, P636
[8]  
Houdret N, 1999, ACTA CLIN BELG, P29
[9]   The HIV-1 viral protein R induces apoptosis via a direct effect on the mitochondrial permeability transition pore [J].
Jacotot, E ;
Ravagnan, L ;
Loeffler, M ;
Ferri, KF ;
Vieira, HLA ;
Zamzami, N ;
Costantini, P ;
Druillennec, S ;
Hoebeke, J ;
Briand, JP ;
Irinopoulou, T ;
Daugas, E ;
Susin, SA ;
Cointe, D ;
Xie, ZH ;
Reed, JC ;
Roques, BP ;
Kroemer, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 2000, 191 (01) :33-45
[10]   A CONTROLLED TRIAL OF BUPRENORPHINE TREATMENT FOR OPIOID DEPENDENCE [J].
JOHNSON, RE ;
JAFFE, JH ;
FUDALA, PJ .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1992, 267 (20) :2750-2755