Predicting cirrhosis risk based on the level of circulating hepatitis B viral load

Cirrhosis develops as a result of hepatic inflammation and subsequent fibrosis in chronic hepatitis B infection. We report on the relationship between hepatitis B viremia and progression to cirrhosis in chronic hepatitis B infection.

This was a population-based prospective cohort study of 3582 untreated hepatitis B-infected patients established in Taiwan from 1991 to 1992. Serum samples were tested for HBV DNA on cohort entry serum samples and the diagnosis of cirrhosis was by ultrasound.

During a mean follow-up time of 11 years, the 3582 patients contributed 40,038 person-years of follow-up evaluation and 365 patients were newly diagnosed with cirrhosis. The cumulative incidence of cirrhosis increased with the HBV-DNA level and ranged from 4.5% to 36.2% for patients with a hepatitis B viral load of less than 300 copies/mL and 10(6) copies/mL or more, respectively (P < .001). In a Cox proportional hazards model adjusting for hepatitis B e-antigen status and serum alanine transaminase level among other variables, hepatitis B viral load was the strongest predictor of progression to cirrhosis relative risk [95% confidence interval] was 2.5 [1.6-3.8]; 5.6 [3.7-8.5]; and 6.5 [4.1-10.2] for HBV-DNA levels >/=10(4) - <10(5); >/=10(5) - <10(6); >/=10(6) copies/mL, respectively.

These data show that progression to cirrhosis in hepatitis B-infected persons is correlated strongly with the level of circulating virus. The risk for cirrhosis increases significantly with increasing HBV-DNA levels and is independent of hepatitis B e-antigen status and serum alanine transaminase level.