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Isoniazid Preventive Therapy, Hepatitis C Virus Infection, and Hepatotoxicity among Injection Drug Users Infected withMycobacterium tuberculosis
Author(s) -
Pankaj Sadaphal,
Jacquie Astemborski,
Neil M.H. Graham,
Laura Sheely,
Margaret Bonds,
Azalia Madison,
David Vlahov,
David L. Thomas,
Timothy R. Sterling
Publication year - 2001
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1086/323896
Subject(s) - isoniazid , medicine , tuberculosis , rifampicin , hepatitis , mycobacterium tuberculosis , elevated transaminases , immunology , hepatitis c virus , latent tuberculosis , discontinuation , coinfection , transaminase , virus , pathology , biology , biochemistry , enzyme
Treatment of latent Mycobacterium tuberculosis infection with isoniazid can cause hepatotoxicity, but the risk of isoniazid-associated hepatotoxicity among persons coinfected with hepatitis C virus (HCV) is unknown. We conducted a prospective study among 146 injection drug users with M. tuberculosis infection and normal baseline hepatic transaminase values who were treated with isoniazid. Of 146 participants, 138 (95%) were HCV-seropositive. Thirty-seven participants (25%) were human immunodeficiency virus (HIV)-seropositive. Thirty-two (22%; 95% confidence interval [CI], 16%-30%) of 146 participants developed transaminase value elevations to >3 times the upper limit of normal. Transaminase value elevation was associated with concurrent alcohol use but not with race, age, presence of hepatitis B surface antigen, HIV-1 infection, or current injection drug use. Isoniazid was withdrawn from 11 participants (8%; 95% CI, 4%-13%). Of 8 deaths during follow-up, none were attributed to isoniazid-associated hepatotoxicity. The risk of transaminase value elevation and drug discontinuation for HCV-infected persons receiving isoniazid was within the range reported for populations with lower HCV prevalence.

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