High viral loads, serum alanine aminotransferase and gender are predictive factors for the development of hepatocellular carcinoma from viral compensated liver cirrhosis.

Abstract

The aims of the present study were to determine the occurrence rate of hepatocellular carcinoma (HCC) and to assess the risk factors for the development of HCC in compensated viral liver cirrhosis. Two hundred and thirty-nine cirrhotic patients (65 hepatitis B surface antigen (HBsAg) positive, 165 hepatitis C virus (HCV) antibody positive (anti-HCV), and nine with both HBsAg and anti-HCV positivity) were studied. The Kaplan-Meier method evaluated by a log-rank test was used to estimate the cumulative probability of HCC development. Independent predictors of HCC development were estimated by using the Cox proportional hazard regression analysis. Dual infection manifested as HBsAg and anti-HCV positive was the highest risk of HCC. Multivariate analysis indicated that anti-HCV positive, HBsAg positive, and lactate dehydrogenase were independent predictors of the development of HCC among individuals with viral cirrhosis. In the HBsAg-positive group, a high-titer of HBV-DNA (more than 3.7 log genome equivalents (LGE)/mL) was most predictive of HCC development. In the anti-HCV-positive group, male gender and a high-titer of HCV-RNA (more than 1.0 Meq/mL) were predictive factors for the development of HCC. Individuals with high viral loads should be monitored for the development of HCC. Clinical efforts at eradicating or reducing the viral load may reduce the risk for HCC.