title: Pathological evolution of hepatitis C virus-"Healthy carriers".
abstract: OBJECTIVE
  To determine factors associated with fibrosis progression in hepatitis C virus (HCV)-infected patients without significant initial pathological lesions.
  
  
  METHODS
  Seventy six untreated HCV-infected patients with initially normal liver as defined by a Knodell score < or = 3, with 2 liver biopsies and detectable HCV-RNA were included. Markers of fibrosis progression were assessed.
  
  
  RESULTS
  Median duration of infection and time between paired biopsies was 13 (95% CI: 1-28) and 4 (95% CI: 2-16) years respectively. Alanine-transaminase (ALT) activity was normal in 43.4% of cases. 50% demonstrated progression of the necro-inflammation and 34% of fibrosis after a median time evolution of 4 years (95% CI: 2-16). The median difference in the necro-inflammation and fibrosis score between biopsies was low, 1.5 and 0.0 respectively. Univariate analysis showed there was no difference between fibrosis activity or evolution according to genotype or viral load. A higher fibrosis progression (P = 0.03) was observed in patients with body mass index (BMI) > 25. Fibrosis progression correlated with the time interval between biopsies (P = 0.01). A significant progression of activity (1.7 vs 0.4, P < 0.05) or fibrosis (0.9 vs 0.0, P < 0.01) was observed in patients with elevated ALT. There was a significant correlation between activity progression and fibrosis progression (P = 0.003). Multivariate analysis demonstrated that fibrosis progression was associated with elevated ALT, BMI > 25 and the time interval between 2 biopsies.
  
  
  CONCLUSIONS
  There is no fibrosis progression in 66% of patients without significant initial histopathological lesion. Fibrosis progression is associated with elevated ALT and BMI > 25.
authors.affiliation: INSERM U785, Centre Hepato-Biliaire, Hopital Paul Brousse, Villejuif, France. rodolphe.sobesky@pbr.aphp.fr
authors.forename: Rodolphe
authors.initials: R
authors.lastname: Sobesky
authors.forename: Pascal
authors.initials: P
authors.lastname: Lebray
authors.forename: Bertrand
authors.initials: B
authors.lastname: Nalpas
authors.forename: Anais
authors.initials: A
authors.lastname: Vallet-Pichard
authors.forename: Helene
authors.initials: H
authors.lastname: Fontaine
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Lagneau
authors.forename: Stanislas
authors.initials: S
authors.lastname: Pol
mesh_terms: D000293:Adolescent; D000328:Adult; D000410:Alanine Transaminase / Q000097:blood; D001706:Biopsy; D015992:Body Mass Index; D002353:Carrier State / Q000821:virology*; D018450:Disease Progression; D005260:Female; D016174:Hepacivirus / Q000235:genetics / Q000472:pathogenicity*; D006526:Hepatitis C / Q000378:metabolism* / Q000473:pathology*; D006801:Humans; D008099:Liver / Q000201:enzymology / Q000473:pathology* / Q000821:virology*; D008103:Liver Cirrhosis / Q000378:metabolism / Q000473:pathology / Q000821:virology; D008137:Longitudinal Studies; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D012367:RNA, Viral / Q000097:blood; D012720:Severity of Illness Index; D019562:Viral Load
chemical_list: D012367:RNA, Viral; D000410:Alanine Transaminase