Abstract and Introduction
Abstract
There is scarce information about the impact of antiviral treatment on subsequent progression of liver fibrosis in HIV-infected patients with chronic hepatitis C who experience different outcomes following peginterferon-ribavirin therapy. We conducted a retrospective study of a cohort of HIV/HCV-coinfected patients with longitudinal assessment of liver fibrosis using elastometry. Patients were split out into four groups according to the prior peginterferon-ribavirin response: sustained virological response (SVR), relapse (R), partial response (PR) and null response (NR). A group of untreated, coinfected patients was taken as control. Significant liver fibrosis progression (sLFP) was defined as a shift from baseline Metavir estimates ≤F2 to F3-F4, or by >30% increase in liver stiffness in patients with baseline F3-F4. Conversely, significant liver fibrosis regression (sLFR) was defined as a shift from baseline Metavir estimates F3-F4 to ≤F2, or by >30% reduction in liver stiffness in patients that kept on F3-F4. A total of 498 HIV/HCV-coinfected patients were examined. They were classified as follows: 138 (27.7%) SVR, 40 (8%) R, 61 (12.2%) PR, 71 (14.3%) NR and 188 (37.8%) naive. After a mean follow-up of 53.3 months, sLFP occurred less frequently in patients with SVR (7.2%) compared with R (25%; P = 0.002), PR (23%; P = 0.002), NR (29.6%; P < 0.001) and naïve (19.7%; P = 0.002). Conversely, sLFR was 26.1% in SVR compared with 10% in R (P = 0.03), 14.8% in PR (P = 0.06), 16.9% in NR (P = 0.07) and 10.6% in naïve (P < 0.001). Sustained clearance of serum HCV-RNA following a course of antiviral treatment is the major determinant of liver fibrosis regression in HIV/HCV-coinfected patients.
Introduction
Chronic hepatitis C virus (HCV) infection is frequently seen in HIV-infected individuals. Although this is particularly true for individuals infected parenterally, such as injecting drug users and recipients of contaminated blood products, an epidemic of sexually transmitted HCV is currently ongoing among homosexual men in large cities in Western countries. HCV-related liver disease is accelerated in the HIV setting, especially in persons with low CD4 counts. Although antiretroviral therapy may ameliorate this effect, it is not completely reversed. Thus, treatment of chronic hepatitis C remains as a priority in HIV/HCV-coinfected patients.
Response to peginterferon plus ribavirin is lower in HIV/HCV-coinfected patients than in HCV-monoinfected individuals. Interestingly, elimination of HCV with antiviral therapy has been associated with improved outcomes, including longer survival, less hepatic events and regression of liver fibrosis in coinfected patients. There is scarce information about the impact of antiviral treatment on subsequent liver fibrosis progression in coinfected patients who experience different modalities of treatment failure following a course of peginterferon plus ribavirin, a question that has been awakened by a recent report claiming a better prognosis for relapsers compared with null responders.