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

UH Iloeje, HI Yang, J Su, CL Jen, SL You, CJ Chen - Gastroenterology, 2006 - Elsevier
UH Iloeje, HI Yang, J Su, CL Jen, SL You, CJ Chen
Gastroenterology, 2006Elsevier
Background & Aims: 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. Methods: 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. Results …
Background & Aims
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.
Methods
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.
Results
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 106 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 ≥104 − <105; ≥105 − <106; ≥106 copies/mL, respectively.
Conclusions
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.
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