Association Between Level of Fibrosis, Rather than Antiviral Regimen, and Outcomes of Patients with Chronic Hepatitis B

2016 Clinical Gastroenterology & Hepatology In press;

BACKGROUND & AIMS: We performed a propensity-score matched analysis to investigate whether entecavir, compared with lamivudine, can reduce risk of hepatocellular carcinoma (HCC) in patients with chronic hepatitis B after adjusting for level of fibrosis. METHODS: We performed a retrospective study of 1079 patients with chronic hepatitis B who received first-line therapy with lamivudine (n=435) or entecavir (n=644) from 2006 through 2013 at Yonsei University College of Medicine in South Korea. Only patients with available liver stiffness value measured by transient elastography were recruited. Liver cirrhosis was diagnosed by ultrasonography. To adjust for the imbalance of patients treated with lamivudine vs entecavir, we performed propensity-score matching (PSM), at a ratio of 1:1, using 7 factors (age, sex, hepatitis B e antigen, alanine aminotransferase, serum albumin, platelet count, and liver stiffness; PSM1) or 8 factors (variables of PSM1 plus ultrasonography measurements of cirrhosis; PSM2). Patients with virologic breakthrough or resistance mutations received rescue therapy. RESULTS: Over the 7 year period, 91 patients developed HCC and 104 had liver-related events in the entire cohort. In multivariate analyses, level of fibrosis, but not antiviral regimen, was independently associated with risk of HCC (P<.05 the psm1 group included pairs of patients and psm2 pairs. similar proportions given lamivudine vs entecavir developed hcc in each model all p>.05). When PSM was applied to patients with liver stiffness measurements =13kPa or >13kPa, patients given lamivudine vs entecavir still had similar cumulative rates of HCC development (all P>.05). CONCLUSION: In a PSM analysis, we associated level of fibrosis, rather than antiviral therapy, with risk of HCC, when patients received appropriate rescue therapy in case of virologic breakthrough or resistance mutations.

Pubmed : 27305847