Objective:To assess the role of different hepatitis C virus (HCV) genotypes in the development of transaminase elevation after treatment with highly active antiretroviral therapy (HAART).
Design:Retrospective cohort study at one referral HIV outpatient clinic.
Methods:HCV genotype was determined in plasma samples from all consecutive HCV-HIV coinfected patients initiating HAART between March 1998 and January 2000. Clinical and laboratory data were recorded during the following 9 months. Severe transaminase elevation was defined as ≥ fivefold increase over upper normal limits (AIDS Clinical Trials Group grades 3 or 4) when baseline alanine transaminase (ALT) and aspartate transaminase (AST) values were normal, and as ≥ 3.5-fold increase above baseline ALT and AST values if they were abnormal.
Results:Twelve of 70 subjects (17%) developed severe transaminase elevation. Their HCV genotypes were distributed as follows: type 1, 5/39 (13%); type 2, 0/3 (0%); type 3, 7/21 (33%); and type 4, 0/7 (0%). The incidence of severe transaminase elevation was significantly higher among subjects with HCV genotype 3 (HCV-3) compared with those with non-type 3 (OR, 4.4 [95%CI, 1.2-16.1]; P = .02). In the multivariate analysis, HCV-3 remained associated with severe transaminase elevation when adjusted for baseline HCV viral load and degree of immune recovery seen during follow-up evaluation.
Conclusions:HCV-3 is an independent risk factor for developing severe transaminase elevation after HAART. HCV genotyping before initiating antiretroviral therapy may be useful for assessing the risk of hepatotoxicity and for choosing the most appropriate drugs to prescribe for HIV-HCV coinfected patients. Given that the best response to interferon plus ribavirin occurs in patients with HCV-3, treatment should be specially encouraged in coinfected persons carrying HCV-3.
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Manuscript received October 22, 2001; accepted February 6, 2002.
© 2002 Lippincott Williams & Wilkins, Inc.