Abstract / Summary
Chronic hepatitis B remains a major cause of cirrhosis and hepatocellular carcinoma worldwide. We investigated whether histologic hepatic steatosis affects hepatitis B virus deoxyribonucleic acid (HBV DNA) suppression in patients receiving antiviral therapy. This retrospective observational study included 307 adult patients with chronic hepatitis B who received tenofovir or entecavir therapy and underwent pretreatment liver biopsy. Demographic, laboratory, virological, radiological, and histopathological data were retrieved from the electronic medical record system. Laboratory parameters included complete blood count, liver function tests, alpha-fetoprotein, renal function tests, and lipid profile. Histopathological evaluation included fibrosis stage, histologic activity index, and hepatic steatosis percentage. Ultrasonographic findings included hepatic steatosis, liver echotexture, and contour. The primary outcome was HBV DNA suppression at 12 months. Long-term virological response was evaluated as time to first HBV DNA suppression during follow-up (maximum 60 months). A total of 307 patients receiving entecavir or tenofovir were included, of whom 258 (84.0%) achieved HBV DNA suppression at 12 months. Patients without suppression had higher baseline aspartate aminotransferase, histologic activity index, histologic steatosis, and baseline log 10 HBV DNA levels (all P < .05). Histologic steatosis ≥5% was more frequent in patients without suppression (42.9% vs 23.6%, P = .005). In multivariable analysis, steatosis ≥5% (odds ratio 0.365, 95% confidence interval [CI] 0.179–0.746; P = .006) and higher baseline log 10 HBV DNA (odds ratio 0.842, 95% CI 0.751–0.944; P = .003) were associated with a lower likelihood of 12-month suppression, with similar findings in the parsimonious sensitivity model. Kaplan–Meier analysis showed delayed suppression with steatosis (log-rank P = .016); however, this association was not significant in the conventional adjusted Cox model (hazard ratio 0.900, 95% CI 0.689–1.175; P = .438), and a significant time-dependent interaction indicated non-proportionality ( P < .001). Histologic steatosis and higher baseline log 10 HBV DNA were associated with a lower likelihood of 12-month HBV DNA suppression. However, an independent longitudinal association with time to suppression was not demonstrated. Residual confounding by unmeasured metabolic factors cannot be excluded.