Levels of serum markers of liver inflammation and fibrosis in patients with chronic hepatitis C virus infection according to HIV status and antiretroviral use

Abbie Connoy, JoLyn Turner, Marina Núñez
AIDS Research and Human Retroviruses 2011, 27 (7): 719-25
Liver disease in patients with chronic hepatitis C virus (HCV) infection has an accelerated course in the presence of human immunodeficiency virus (HIV) coinfection. Some data suggest that HIV suppression achieved with highly active antiretroviral therapy (HAART) ameliorates HCV-related liver disease progression. The aim of this study was to test if there is overexpression of serum markers of liver inflammation and fibrosis in HIV-HCV-coinfected patients and if the effect is counteracted by HAART. In a pilot, cross-sectional, and comparative study serum markers of liver inflammation (CK-18 and HGF) and fibrosis (HGF, MMP-2, and TIMP-1) were measured via ELISA in HIV-infected patients off and on HAART, HCV monoinfected, HIV-HCV coinfected off and on HAART, and controls (10 per group). HIV-HCV-coinfected off HAART patients with low CD4 counts had higher levels of M30, HGF, and MMP-2 than HIV-HCV-coinfected on HAART. HCV coinfection predicted higher levels of MMP-2 [B 65.82 (95% CI 3.86-127.78); p = 0.04], HGF [B 520.22 (95% CI 123.65-916.78); p = 0.01] and M30 [B 128.02 (95%CI 16.39-239.64); p = 0.03]. HAART use was a predictor of lower levels of MMP2 [B -83.18 (95%CI (-146.8) - (-19.52)); p = 0.01] and M30 [B -112.9 (95% CI (-221.3) - (-4.52)); p = 0.04]. Other factors analyzed including alcohol intake ware not associated with the studied markers. In conclusion, serum markers of hepatic inflammation and fibrosis are overexpressed in HIV-HCV-coinfected patients with advanced immunosuppression, while HAART has a "protective" effect.

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