Eradication of Hepatitis C Virus Reduces the Risk of Hepatocellular Carcinoma in Patients with Compensated Cirrhosis
- نوع فایل : کتاب
- زبان : انگلیسی
- مؤلف : Jose´ Velosa Fa´tima Serejo Rui Marinho Joana Nunes Helena Glo´ria
- چاپ و سال / کشور: 2011
Description
Background The effect of a sustained virological response (SVR) to interferon (IFN) on clinical outcomes of hepatitis C virus (HCV)–related cirrhosis is controversial. Aims: Evaluate the effect of SVR to IFN on the incidence of hepatocellular carcinoma (HCC) and mortality in patients with compensated HCV-induced cirrhosis. Methods A cohort of 130 consecutive patients (92 men, mean age 51.7 years) with histologically proven cirrhosis who received one or more courses of IFN monotherapy or combination therapy with ribavirin were analyzed. SVR was defined as undetectable serum HCV RNA by real-time polymerase chain reaction (PCR) 24 weeks after IFN discontinuation. HCC was assessed by alfa-fetoprotein and ultrasound every 6 months. Predictors of clinical outcomes, defined as HCC, orthotopic liver transplantation (OLT) and mortality, were assessed by Cox regression analysis. Results The mean follow-up was 6.4 ± 4.0 years (range 1–18). HCC developed in 21 patients: one with SVR versus 20 with non-SVR (P = 0.017). Logistic regression analysis showed that non-SVR (odds ratio [OR] = 27.0; confidence interval [CI], 1.6–452.1), male (OR = 11.6; CI, 1.8–75.4), and greater number of treatments (OR = 4.7; CI, 1.4–16.0) increased the probability of HCC development. Multivariate analysis found that SVR was associated with lower risk of HCC (HR 0.09; CI, 0.01–0.77), OLT (HR 0.04; CI, 0.003–0.63) and any event (HR 0.11; CI, 0.02–0.46) as compared to non-SVR. Conclusions In compensated HCV-related cirrhosis, SVR markedly reduces the risk of HCC and improves survival. Clearance of the virus should be intensively attempted in these patients.
Dig Dis Sci (2011) 56:1853–1861 DOI 10.1007/s10620-011-1621-2 Received: 27 September 2010 / Accepted: 6 February 2011 / Published online: 5 March 2011
