Factors affecting liver fibrosis in human immunodeficiency virus- and hepatitis C virus-coinfected patients: Impact of protease inhibitor therapy

Hepatitis C virus (HCV)-related liver fibrosis progression is accelerated i n human immunodeficiency virus (HIV)-infected patients. The effect of prote ase inhibitor (PI) therapy on liver fibrosis is unknown. The aim of this wo rk was to analyze the impact of PI therapy on HCV-related liver fibrosis in HIV/HCV coinfected patients. We evaluated in a longterm follow-up retrospe ctive cohort study the influence of antiretroviral therapy containing PI on liver fibrosis in 182 consecutive HIV/HCV coinfected patients. At liver bi opsy, 63 patients had received PI and 119 patients had never been treated w ith PI. Relationships between liver histologic features, age, alcohol consu mption, CD4 cell count, HIV-RNA load, and antiretroviral regimens were anal yzed. Liver fibrosis stage was lower in patients receiving PIs by compariso n with patients who had never received PIs (P = .03). The 5-, 15-, and 25-y ear cirrhosis rates were 2% versus 5%, 5% versus 18%, and 9% versus 27%, re spectively, in patients who had received PIs compared with PI-untreated pat ients (P = .0006). Multivariate analysis identified 4 independent predictor s of progression to cirrhosis: absence of protease inhibitor therapy (relat ive risk [RR] = 4.74, 95% confidence interval [CI], 1.34-16.67), heavy alco hol consumption ( greater than or equal to 50 g daily) (RR = 4.71, 95% CI, 1.92-11.57), low CD4 cell count (< 200/muL) (RR = 2.74, 95% CI, 1.17-6.41), and age at HCV contamination ( greater than or equal to 20 years) (RR = 2. 37, 95% CI, 1.04-5.38). In conclusion, protease inhibitor therapy might not accelerate progression to HCV-related cirrhosis. Furthermore, chronic use of antiretroviral therapy containing PI together with reduction of alcohol consumption and maintenance of high CD4 count could have a beneficial impac t on liver fibrosis progression in HIV/HCV coinfected patients.