Leptin Has No Role in Determining Severity of Steatosis and Fibrosis in Patients With Chronic Hepatitis C

Giannini, Edoardo; Ceppa, Paola; Botta, Federica; Mastracci, Luca; Romagnoli, Paola; Comino, Ilaria; Pasini, Andrea; Risso, Domenico; Lantieri, Pasquale B.; Icardi, Giancarlo; Barreca, Tommaso; Testa, Roberto
November 2000
American Journal of Gastroenterology;Nov2000, Vol. 95 Issue 11, p3211
Academic Journal
OBJECTIVE: The presence of steatosis is a common histological finding in patients with chronic hepatitis C (CHC). The causes of the severity of this condition arc not yet clear, although both metabolic and viral factors supposedly are involved. In this study our aim was to examine the possible influence that leptin levels, hepatitis C virus (HCV) RNA levels, and hepatitis G virus (HGV) infection have on the severity of steatosis and on the presence and degree of fibrosis in patients with CHC. METHODS: One hundred eighty-two CHC patients with histological findings of steatosis were chosen from among a cohort of patients referred to our center for staging of liver disease. Among them 48 CHC patients were accurately selected so as to rule out possible confounding factors for the presence of steatosis (diabetes mellitus, hyperlipemia, obesity, alcohol). Leptin levels, HCV RNA levels, and HCV genotype, and the presence of HGV RNA were assessed in these patients and related to histological findings. RESULTS: We found that leptin levels in CHC patients were similar to those in healthy subjects. No relationship was found between leptin levels and severity of steatosis. HCV RNA levels, HCV genotype, and the presence of HGV infection were no different among CHC patients with various degrees of steatosis. Leptin was not related to different degrees of fibrosis, whereas higher viral load was the only parameter associated to higher fibrosis scores. CONCLUSIONS: These findings suggest that the degree of steatosis in patients with CHC does not seem to depend on serum leptin levels or on viral factors, at least as far as HCV viremia and genotype and HGV infection are concerned. The severity of fibrosis does not seem to be influenced by leptin levels, whereas HCV viral load does seem to play some role.


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