title: Leptin has no role in determining severity of steatosis and fibrosis in patients with chronic hepatitis C.
abstract: 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 are 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.
authors.affiliation: Department of Internal Medicine, University of Genoa, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Giannini
authors.forename: P
authors.initials: P
authors.lastname: Ceppa
authors.forename: F
authors.initials: F
authors.lastname: Botta
authors.forename: L
authors.initials: L
authors.lastname: Mastracci
authors.forename: P
authors.initials: P
authors.lastname: Romagnoli
authors.forename: I
authors.initials: I
authors.lastname: Comino
authors.forename: A
authors.initials: A
authors.lastname: Pasini
authors.forename: D
authors.initials: D
authors.lastname: Risso
authors.forename: P B
authors.initials: PB
authors.lastname: Lantieri
authors.forename: G
authors.initials: G
authors.lastname: Icardi
authors.forename: T
authors.initials: T
authors.lastname: Barreca
authors.forename: R
authors.initials: R
authors.lastname: Testa
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D005234:Fatty Liver / Q000473:pathology*; D005260:Female; D018067:Flaviviridae / Q000235:genetics; D016174:Hepacivirus / Q000302:isolation & purification; D019698:Hepatitis C, Chronic / Q000097:blood / Q000473:pathology*; D006525:Hepatitis, Viral, Human / Q000473:pathology; D006801:Humans; D020738:Leptin / Q000097:blood*; D008099:Liver / Q000473:pathology*; D008103:Liver Cirrhosis / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D012720:Severity of Illness Index; D019562:Viral Load
chemical_list: D020738:Leptin; D012367:RNA, Viral