title: Association between leptin, metabolic factors and liver histology in patients with chronic hepatitis C.
abstract: BACKGROUND
  Steatosis is common in hepatitis C virus (HCV)-infected patients and likely accelerates fibrosis progression. Leptin, the peptide product of the obesity gene (ob), has been implicated in hepatic fibrogenesis; circulating levels of leptin correlate with body fat mass. The objective of the present study was to determine the clinical and histological correlates of serum leptin in HCV-infected patients, and to determine its utility in predicting liver histological lesions.
  
  
  METHODS
  In 62 patients with chronic HCV, serum leptin was measured using a commercially available immunoassay. Associations between leptin, metabolic parameters, and severe hepatic fibrosis (stages 2 to 4) and steatosis (30% or greater) were determined. The utility of leptin in predicting liver histology was determined using receiver operating characteristic (ROC) curves.
  
  
  RESULTS
  The median body mass index (BMI) was 23.2 kg/m2 (range 17.7 kg/m2 to 35.6 kg/m2); 16% of patients (n=10) had HCV genotype 3. Severe fibrosis and steatosis were present in 23% and 13% of patients, respectively. Leptin was strongly correlated with the BMI, and its levels were higher in women. BMI-corrected leptin levels were not independently associated with severe fibrosis but were significantly associated with steatosis (OR of 1.07; 95% CI 1.01 to 1.04). On it own, leptin was poorly predictive of severe steatosis (area under the ROC curve was 0.64; 95% CI 0.42 to 0.87). However, its accuracy improved with the addition of HCV genotype (area under the ROC curve was 0.86; 95% CI 0.72 to 1.00; P=0.07).
  
  
  CONCLUSIONS
  As observed in the non-HCV setting, serum leptin correlates with BMI; higher leptin levels are found in women than men with chronic HCV. Serum leptin is a poor predictor of HCV-related fibrosis but may play a role in predicting steatosis when combined with HCV genotype.
authors.affiliation: Department of Medicine, University of Calgary, Calgary, Canada. rpmyers@ucalgary.ca
authors.forename: Robert P
authors.initials: RP
authors.lastname: Myers
authors.forename: Djamila
authors.initials: D
authors.lastname: Messous
authors.forename: Thierry
authors.initials: T
authors.lastname: Poynard
authors.forename: Francoise
authors.initials: F
authors.lastname: Imbert-Bismut
mesh_terms: D000328:Adult; D000368:Aged; D015992:Body Mass Index; D015331:Cohort Studies; D003430:Cross-Sectional Studies; D005234:Fatty Liver / Q000097:blood / Q000473:pathology / Q000821:virology; D005260:Female; D019698:Hepatitis C, Chronic / Q000097:blood* / Q000150:complications / Q000473:pathology*; D006801:Humans; D020738:Leptin / Q000097:blood*; D008103:Liver Cirrhosis / Q000097:blood / Q000473:pathology / Q000821:virology; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D012737:Sex Factors
chemical_list: D020738:Leptin