Objectives: It is still debated whether hepatitis B virus (HBV) infection is associated with the development of diabetes. Our primary objective was to determine whether insulin resistance is associated with HBV-induced histologic severity.
Methods: This study included consecutive 80 nondiabetic, noncirrhotic patients with HBV infection who underwent liver biopsy. We evaluated the relationship between histologic findings and clinical parameters and insulin resistance determined by the homeostasis model assessment (HOMA-IR).
Results: Patients with minimal fibrosis (stage 0 or 1) had significantly higher levels of insulin and HOMA-IR (P = 0.004, P = 0.028, respectively) compared with matched healthy controls. HOMA-IR is independently associated with body mass index (coefficient, 0.16; 95% confidence interval, CI, 0.03-0.28) but not with HBV-induced histologic activity or fibrosis. Insulin resistance was not significantly different among patients with or without significant fibrosis (stage 2 or 3). In multivariate analysis, Hepatitis B e antigen (HBeAg) positivity (odds ratio, OR, 0.04; 95% CI, 0.01-0.31) and portal/periportal inflammation (OR, 18.6; 95% CI, 3.9-88.2) were independent predictors of significant fibrosis.
Conclusions: The observed hyperinsulinemia in HBV-infected patients seems to be from altered insulin metabolism rather than HBV-specific effects. Insulin resistance is not associated with significant fibrosis. The data suggest that hepatic fibrosis in HBV-infected patients is attributable to the virus-induced liver injury, but not to insulin resistance.