Treatment of Chronic Hepatitis C in HIV-infected Patients With Compensated Liver Cirrhosis

L. Martín-Carbonero; P. Tuma, E. Vispo; J. Medrano, P. Labarga; J. González-Lahoz; P. Barreiro; V. Soriano


J Viral Hepat. 2011;18(8):542-548. 

In This Article

Abstract and Introduction


The greatest benefit of hepatitis C virus (HCV) therapy is seen in cirrhotics attaining sustained virological response (SVR). However, concerns about toxicity and poorer responses often discourage treatment of cirrhotics. This may be particularly relevant in HIV–HCV-coinfected patients, in whom progression of liver fibrosis is faster and treatment responses lower. This is a retrospective analysis of HIV–HCV-coinfected patients who had received peginterferon–ribavirin therapy at our institution. Individuals naïve for interferon in whom liver fibrosis had been assessed using elastometry within the year before being treated were chosen. Response rates and toxicities were compared in cirrhotics (>14.5 KPa) and noncirrhotics. Patients with previous liver decompensation were excluded. Overall, 41 cirrhotics and 190 noncirrhotics entered the study. Groups were similar in age, gender, HCV genotypes and baseline serum HCV-RNA. SVR occurred at similar rates in cirrhotic and noncirrhotics, either considered by intention-to-treat (39%vs 45%; P = 0.4) or as treated (50%vs 52%, P = 0.8). In multivariate analysis (odds ratio, 95% CI, P), SVR was associated with HCV genotypes 2–3 (5, 2.9–11, <0.01) and lower serum HCV-RNA (2, 1.4–3.03 for every log decrease, <0.01) but not with cirrhosis (1.2, 0.4–3.6, 0.6). Treatment discontinuations because of adverse events tended to be more common in cirrhotics than in noncirrhotics (17%vs 12%; P = 0.2), but only severe thrombocytopenia was more frequent in cirrhotics than in non-cirrhotics (20%vs 3% at week 24; P < 0.01). Response to peginterferon–ribavirin therapy is similar in HIV–HCV coinfected patients with and without liver cirrhosis. Therefore, treatment must be encouraged in all compensated cirrhotic patients, although closer monitoring and management of side effects, mainly thrombocytopenia, may be warranted.


Liver disease is currently one of the leading causes of morbidity and mortality among HIV-infected patients in western countries.[1] Chronic hepatitis C virus (HCV) infection accounts for the majority of cases of hepatic illness, which explains why HCV treatment has become a priority in this population[2]

Cirrhosis is the last stage of chronic hepatitis C. It is histologically defined by dense bands of fibrosis surrounding regenerative nodules[3,4] and clinically characterized by the development of portal hypertension and impaired synthetic liver function.[5] In addition, advanced liver fibrosis predispose to hepatocellular carcinoma.[6] Overall, 30% of patients with chronic hepatitis C develop cirrhosis long life. Furthermore, a quarter of them will experience clinical liver decompensation events.[7] Faster progression to cirrhosis and increased rate of decompensation events, liver cancer and liver-related deaths have been demonstrated in patients with chronic hepatitis C coinfected with HIV.[8–11]

Clearance of HCV following successful treatment prevents liver fibrosis progression and consequently reduces the risk of liver failure, liver-related death and hepatocellular carcinoma.[12–15] While patients with compensated cirrhosis will benefit the greatest from curing chronic hepatitis C, concern exists that this subset of patients may respond less to therapy and experience more side effects.[16,17] Information on the efficacy of peginterferon–ribavirin therapy in HIV-infected patients with compensated liver cirrhosis is scarce and often limited by the small size of study populations and use of suboptimal treatment regimens. The aim of our study was to compare the efficacy and safety of current HCV therapy in a group of coinfected patients, in whom the subset with liver cirrhosis was largely represented.


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