Serum leptin levels correlate with hepatic steatosis in chronic hepatitis C

Abstract Objectives Hepatic steatosis (HS) has been related to obesity and fibrosis in chronic hepatitis C (CHC). The aim of this study was to determine the role of leptin system in HS development. Methods Patients (n = 131) with biopsy-proven CHC, positive HCV RNA, and raised ALT were enrolled. Body mass index, percentage of body fat by skin fold measurement, and bioelectrical impedance analysis was calculated and serum leptin concentration measured. Intrahepatic HCV RNA, HS, necroinflammatory activity, and fibrosis were determined in liver biopsy tissue. Results HS was present in 63 patients (48.1%). Steatosis was evident in 32 of 91 patients (35.2%) infected with genotype 1 and in 22 of 27 patients (81.5%) with genotype 3a ( p r = 0.78; p p = 0.038), leptin levels (OR = 1.09, 95% CI = 1.03–1.17, p = 0.008) and fibrosis (OR = 9.86, 95% CI = 2.11–5.86, p = 0.03) as independent variables of HS development. Conclusions Hepatic steatosis was related to genotype, fibrosis degree, and serum leptin levels. Genotype 3 seems to have a viral specific steatogenic effect. Leptin seems to be a link between obesity and steatosis development in CHC genotype 1–infected patients.