title: Steatosis and bile duct damage in chronic hepatitis C: distribution and relationships in a group of Northern Italian patients.
abstract: OBJECTIVE
  Hepatitis C virus (HCV) related disease follows a long, benign course and most affected patients have mild disease. Liver biopsy is mandatory to grade and stage the disease. Characteristic, though non-specific, HCV histological lesions such as bile duct damage and steatosis have been singled out but their association with non-histological parameters has not been completely defined. Our aim was to study the relationships among these histological lesions and clinical, biochemical, functional and virological characteristics in a group of Northern Italian patients with chronic hepatitis.
  
  
  METHODS
  We studied 172 patients with HCV-related chronic hepatitis. Patients were divided into groups on the basis of histology including bile duct damage and steatosis. Clinical, biochemical, functional and virological profiles were related to histological findings.
  
  
  RESULTS
  Histological grading and staging of disease increased as the age of patients increased. Steatosis was present in 70% of our patients and was related to a higher degree of fibrosis and to decreased functional activity. The prevalence of bile duct damage was 20%. This lesion was present in older patients with higher staging and impaired liver function. Biochemically it was associated with an increase in aspartate aminotransferase, gammaglutamyltranspeptidase, alkaline phosphatase, and total bilirubin.
  
  
  CONCLUSIONS
  In the population we studied, HCV chronic hepatitis was predominantly a mild disease. Moreover both steatosis and bile duct damage were also mild. Steatosis was associated with fibrosis and this might influence liver metabolic function. Bile duct lesions were found in older patients with advanced disease showing biochemical evidence ofcholestasis. The molecular role HCV might play in the pathogenesis of these histological features should be addressed in further studies.
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: A
authors.initials: A
authors.lastname: Fasoli
authors.forename: P
authors.initials: P
authors.lastname: Romagnoli
authors.forename: E
authors.initials: E
authors.lastname: Cresta
authors.forename: V
authors.initials: V
authors.lastname: Venturino
authors.forename: D
authors.initials: D
authors.lastname: Risso
authors.forename: G
authors.initials: G
authors.lastname: Celle
authors.forename: R
authors.initials: R
authors.lastname: Testa
mesh_terms: D000328:Adult; D000469:Alkaline Phosphatase / Q000097:blood; D001219:Aspartate Aminotransferases / Q000097:blood; D001649:Bile Duct Diseases / Q000097:blood / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology*; D001652:Bile Ducts / Q000473:pathology; D001663:Bilirubin / Q000097:blood; D005234:Fatty Liver / Q000097:blood / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification / Q000235:genetics / Q000276:immunology; D018937:Hepatitis C Antibodies / Q000097:blood; D019698:Hepatitis C, Chronic / Q000097:blood / Q000150:complications* / Q000453:epidemiology / Q000473:pathology; D006801:Humans; D007558:Italy / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D012367:RNA, Viral / Q000097:blood; D020133:Reverse Transcriptase Polymerase Chain Reaction; D017678:Sex Distribution; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D018937:Hepatitis C Antibodies; D012367:RNA, Viral; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000469:Alkaline Phosphatase; D001663:Bilirubin