To assess the factors associated with liver fibrosis in HIV and hepatitis C virus (HIV/HCV) coinfected patients eligible for anti-HCV therapy, researchers performed an observational, single centre, cross-sectional study of 180 HIV/HCV coinfected patients who underwent liver biopsy between May 1998 and November 2001.

A total of 126 patients with a known date of HCV infection were evaluated. Liver fibrosis was defined as a Knodell stage of fibrosis 1-4.

The mean age was 36.7 (3.8) years, 81% were male and had a mean age of 20.5 (3.8) years at HCV infection. Mean CD4 cell count and plasma HIV-1 RNA load at the time of biopsy were 552 cell/mm3 (239) and 2.5 log10 (0.9), respectively.

One hundred and eighteen patients had been on antiretroviral therapy (ART) for a median of 45 months (Q1-Q3: 21-75) and 84 on protease inhibitor for a median of 12.0 months (Q1-Q3: 0-29.5); 55 had an AIDS event or a CD4 cell count nadir < 200 cells/mm3 prior to biopsy.

Median histological activity index was 6 and 27% had a Knodell stage of fibrosis 0. On the multivariate analysis time on ART, CD4 cell count at the time of liver biopsy, age at HCV infection acquisition and alcohol intake (> 50 g/day) were associated with liver fibrosis.

The authors conclude: “ART should be a priority in HIV-HCV coinfected patients eligible for anti-HCV treatment as it is a protective factor for liver fibrosis.”

Source: HIVandHepatitis.com

http://www.hivandhepatitis.com/hiv_hcv_co_inf/081503a.html

Ref: Tural C and others. Time on antiretroviral therapy is a protective factor for liver fibrosis in HIV and hepatitis C virus (HCV) co-infected patients. Journal of Viral Hepatitis 10(2): 118-125. March 2003.

© Copyright 2002 by HIV and Hepatitis.com. All Rights Reserved. Reproduction for personal or educational use is encouraged and does not require permission. Written permission is required to re-print copyrighted articles but is almost always granted (email publisher@HIVandHepatitis.com).

comment

One hypothesis would be that antiretroviral therapy improves immune function and enables the body to control HCV better, achieving a situation similar to monoinfected patients.

This may slow down the fibrosis rate, as coinfected patients otherwise show a more rapid progression of fibrosis. This study confirms earlier data from Benhamou published in Hepatology in 2000.