With the introduction of highly active antiretroviral therapy in 1996, liver disease has emerged as an important cause of morbidity and mortality in HIV/HCV-coinfected patients. In 2000, RIBAVIC HC02 trial, a randomized controlled trial (the ANRS HC02 RIBAVIC study) comparing pegylated interferon alfa-2b plus ribavirin vith conventional interferon alfa-2b plus ribavirin was conducted. In order to describe the effect of interferon plus ribavirin-based therapies on the incidence of long-term clinical outcomes in HIV/HCV-coinfected patients, a prospective cohort study was performed from the patients included in the ANRS HC02 RIBAVIC trial in 2001. The RIBAVIC trial and the cohort contribute to show these results : - HCV viral load kinetics could differ according to the choice of HAART regimen. - the prevalence (61%) and risk factors for steatosis are similar to that observed in HCV-monoinfected patients. None of the characteristics of HIV infection, including antiretroviral therapy, is independently associated with steatosis. - the rate of sustained virological response is lower in HIV/HCV-coinfected patients (27%) than in HCV-monoinfected patients - the rate of non response (HCV RNA decline of less than 2 logs at 12 weeks of peginterferon and ribavirin combination therapy) is high, ranging from 29% to 33% (14% in HCV-monoinfected patients). The potential loss of ribavirin efficacy on HCV during concomitant use of NRTIs, such abacavir, is suspected. - the best positive and negative predictive values of sustained virological response (SVR) were respectively obtained with an undetectable HCV RNA at W4 (97%) and with more than a 2 log10 decrease at W12 (99%). The HCV viral load decrease at week 2 and week 4 was significantly slower in relapsing patients than in patients with sustained virological response. - During anti-HCV therapy, 1- severe anemia occurred in 15.9% of patients and was significantly higher in patients receiving zidovudine-based HAART ; 2- severe weight loss (> 10% of baseline weight) is frequent (28%) and could be one of the first clinical sign of a mitochondrial toxicity; 3- markers of advanced liver fibrosis and not neutropenia are predictors of increased susceptibility to bacterial infections 4- concomitant treatment with didanosine and interferon-2b or peg-interferon-2b plus ribavirin is associated with an increase risk of symptomatic mitochondrial toxicity, hepatic decompensation and fibrosis worsening.
