A few studies have assessed the observed fibrosis progression between serial liver biopsies (LB) in human immunodeficiency virus (HIV) / hepatitis C virus (HCV)-coinfected patients. Approximately half of the patients progressed at least one fibrosis stage over a short period of time. The risk factors for this fast progression need clarification. Because of this, we evaluated the observed fibrosis progression rates of HIV/HCV-coinfected patients and the risk factors for accelerated progression. Overall, 135 HIV-infected patients with positive serum HCV RNA, without other possible causes of liver disease, who underwent two LB, separated at least by 1 year, were included in this retrospective cohort study. The median (Q1-Q3) time between both LBs was 3.3 (2.0-5.2) years. Patients showed the following changes in fibrosis stage: regression >1 stage: 23 (17%), no change: 52 (39%), progression 1 stage: 38 (28%), and progression >2 stages: 22 (16%). Seventeen (13%) patients had cirrhosis in the second biopsy. Factors independently associated with progression >1 stage were undetectable plasma HIV RNA during the follow-up (relative risk [RR] [95% confidence interval, 95% CI] 0.61 [0.39-0.93], P ؍ 0.03), moderate-to-severe lobular necroinflammation (1.77 [1.16-2.7], P ؍ 0.009), time between biopsies (1.11 [1.08-1.2], P ؍ 0.01), and end of treatment response to anti-HCV therapy (0.41 [0.19-0.88], P ؍ 0.02). Conclusion: Fibrosis progresses with high frequency in HIV/HCV-coinfected patients over a period of time of 3 years. Absent-to-mild lobular necroinflammation at baseline, achievement of response with anti-HCV treatment, and effective antiretroviral therapy are associated with slower fibrosis progression. (HEPATOLOGY 2009;50:1056-1063.)
T he natural course of chronic hepatitis C virus (HCV) is accelerated in human immunodeficiency virus (HIV) infection. 1 Low CD4 cell counts, lack of exposure to antiretroviral therapy (ART), and advanced liver disease are risk factors for liver events and mortality in cohort studies. [1][2][3][4][5] Particularly, CD4 cell recovery and suppression of HIV replication after starting highly active antiretroviral therapy (HAART) are predictors of survival free of complications of cirrhosis. 5 Most data on liver fibrosis progression in HIV and HCV coinfection come from cross-sectional studies that relied on a single liver biopsy. [6][7][8][9][10][11] In those studies, the date of HCV infection is usually estimated as the date of the first use of injection drugs. At HCV infection, it is assumed that liver fibrosis is absent. The majority of the duration of HCV infection was not observed, and factors that could influence fibrosis progression were only collected during a relatively short period of the entire course of HCV infection. These assumptions are probably one reason for the conflicting results of those studies, especially regarding the effect of ART on fibrosis progression. [6][7][8][9][10][11] Serial liver biopsy studies may have some advantages over single liver biopsy studies. Changes in fibrosis stage are observed between two dates, and fibrosis at the initial date is known. Thus, the estimations and assumptions of cross-sectional studies on fibrosis progression are not made. Additionally, factors that could influence fibrosis progression are observed during the period of time between biopsies, and are more easily and reliably gathered.