title: Role of a cirrhosis risk score for the early prediction of fibrosis progression in hepatitis C patients with minimal liver disease.
abstract: OBJECTIVE
  Fibrosis progression in patients with chronic hepatitis C (CHC) is highly variable. A Cirrhosis Risk Score (CRS) based on seven genetic variants has been recently developed for identifying patients at risk for cirrhosis. The objective of this study was to assess the role of the CRS for the early prediction of fibrosis progression in CHC patients with mild liver fibrosis. In addition, we evaluated the potential benefit, for prediction accuracy, of a recently described non-invasive fibrosis staging assay, the Enhanced Liver Fibrosis (ELF) test.
  
  
  METHODS
  Two separate cohorts of HCV patients (Brussels, Belgium/Hannover, Germany) were retrospectively analyzed. Only patients with a fibrosis Ishak or METAVIR score of F0-F1 at baseline were included. Patients were classified as progressors if they showed an increase ≥2 fibrosis stages at the second histological evaluation after a follow-up ≥5years. The CRS was calculated locally. Genotyping was performed by PCR and oligonucleotide ligation with the resulting signal detected with a Luminex® 200TM and computer analysis.
  
  
  RESULTS
  In Brussels, 12/25 patients progressed (48%); similarly in Hannover, 16/31 (52%) patients progressed. In both sample sets, the CRS was significantly associated with fibrosis progression (p=0.050 in Brussels; p=0.018 in Hannover). The ELF test was only a significant predictor in Hannover (p=0.015). In multivariate analysis the CRS remained the only variable associated with fibrosis progression (odds-ratio=2.23, 95%CI 1.21-4.11 p=0.01).
  
  
  CONCLUSIONS
  Although conducted on a limited number of patients, this study in two independent centres confirms that the CRS predicts fibrosis progression in initially mild CHC.
authors.affiliation: Université Libre de Bruxelles, Brussels, Belgium.
authors.forename: Eric
authors.initials: E
authors.lastname: Trépo
authors.forename: Andrej
authors.initials: A
authors.lastname: Potthoff
authors.forename: Pierre
authors.initials: P
authors.lastname: Pradat
authors.forename: Rakesh
authors.initials: R
authors.lastname: Bakshi
authors.forename: Bradford
authors.initials: B
authors.lastname: Young
authors.forename: Robert
authors.initials: R
authors.lastname: Lagier
authors.forename: Christophe
authors.initials: C
authors.lastname: Moreno
authors.forename: Laurine
authors.initials: L
authors.lastname: Verset
authors.forename: Richard
authors.initials: R
authors.lastname: Cross
authors.forename: Delphine
authors.initials: D
authors.lastname: Degré
authors.forename: Arnaud
authors.initials: A
authors.lastname: Lemmers
authors.forename: Thierry
authors.initials: T
authors.lastname: Gustot
authors.forename: Pascale
authors.initials: P
authors.lastname: Berthillon
authors.forename: William
authors.initials: W
authors.lastname: Rosenberg
authors.forename: Christian
authors.initials: C
authors.lastname: Trépo
authors.forename: John
authors.initials: J
authors.lastname: Sninsky
authors.forename: Michael
authors.initials: M
authors.lastname: Adler
authors.forename: Heiner
authors.initials: H
authors.lastname: Wedemeyer
mesh_terms: D015331:Cohort Studies; D018450:Disease Progression; D005260:Female; D014644:Genetic Variation; D019698:Hepatitis C, Chronic / Q000145:classification / Q000150:complications* / Q000235:genetics / Q000473:pathology; D006801:Humans; D008103:Liver Cirrhosis / Q000145:classification / Q000209:etiology* / Q000235:genetics / Q000473:pathology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D020641:Polymorphism, Single Nucleotide; D012189:Retrospective Studies; D012307:Risk Factors