Effect of antiretroviral drugs on liver fibrosis in HIV-infected patients with chronic hepatitis C:: harmful impact of nevirapine

Background: The hepatotoxicity of highly active antiretroviral therapy (HAART) could enhance liver fibrosis in HIV/Hepatitis C virus (HCV)-coinfected patients. Moreover, HAART-related immune restoration could lessen HCV-associated liver damage. The data on the effect of protease inhibitors (PI) on liver fibrosis are scant and contradictory. No information is available on the relationship between non-nucleoside analogue therapy and liver fibrosis in co-infected patients. Objective: To investigate the associations between the use of different antiretroviral drugs and the liver fibrosis in patients with HIV and HCV infections. Design: Cross-sectional study. Methods: All HIV/HCV co-infected patients with an available liver biopsy and known or estimated duration of HCV infection seen at a Infectious Diseases Unit were included in the study. The fibrosis stage and the fibrosis progression rate were evaluated. Results: The inclusion criteria were fulfilled by 152 patients. Age at HCV infection < 20 years [adjusted odds ratio (AOR), 0.39; 95% confidence interval (Cl), 0.190.82], PI-based HAART (AOR, 0.39; 95% Cl, 0.19-0.78) and nevirapine-based HAART (AOR, 2.56; 95% Cl, 1.02-6.58) were associated with fibrosis stage greater than or equal to F3. The variables associated with fibrosis progression rate > 0.2 units/year were age at HCV infection < 20 years (AOR, 0.23; 95% Cl, 0.1-0.52), CD4 cell counts less than or equal to 250 x 10(6)/l at liver biopsy (AOR, 2.8; 95% Cl, 1.1-7.1), PI-based HAART (AOR, 0.39; 95% Cl, 0.2-0.8) and nevirapine-based HAART (AOR, 3.82; 95% Cl, 1.9-7.6). Conclusions: HAART regimens including nevirapine are associated with faster liver fibrosis progression in HIV-infected patients with chronic hepatitis C. In contrast, patients on PI as the backbone of potent antiretroviral therapy are more likely to show less liver fibrosis. (C) 2004 Lippincott Williams Wilkins.