title: Outcome of liver disease in a large cohort of histologically proven chronic hepatitis C: influence of HCV genotype.
abstract: OBJECTIVE
  To assess the influence of hepatitis C virus (HCV) genotypes on the clinical outcome of liver disease, we analysed 2,307 patients.
  
  
  RESULTS
  The most frequently represented genotypes were 1b (40%) and 2 (28.1%). Patients with these genotypes had a median age higher than patients with other genotypes (P< 0.01). The overall survival of subjects with genotype 1b was poorer than the survival of patients with other genotypes (P< 0.01). Liver cirrhosis was found in 280 patients (12.1%), and type 1b was the most represented isolate among them (P< 0.01). Sixty-two patients (22%) developed hepatocellular carcinoma (HCC) during a follow-up of 1481.8 cumulative years (estimated crude incidence rate, 4.1 cases per 100 person-years for all cirrhotics; 5.9 cases for genotype 1a; 4.5 cases for genotype 1b; and 2.8 cases for genotypes non-1). Considering the whole population of 2,307 patients, only genotype 1b was associated significantly with both cirrhosis and the development of HCC. One hundred and nineteen cirrhotic patients underwent treatment with interferon in uncontrolled studies. Interferon therapy was associated with both better survival (P< 0.01) and a lower cumulative hazard for HCC (P< 0.01).
  
  
  CONCLUSIONS
  Genotype 1b was associated with a poorer prognosis, probably because it leads to cirrhosis and consequently to HCC development. However, our data did not confirm genotype 1b as an independent risk factor for HCC in liver cirrhosis, which plays a major role in carcinogenesis. Interferon should be considered as a useful strategy in cirrhosis for improvement of survival and reduction of HCC risk.
authors.affiliation: Department of Internal Medicine, Sondrio Hospital, Italy. anabasis@tin.it
authors.forename: L
authors.initials: L
authors.lastname: Roffi
authors.forename: A
authors.initials: A
authors.lastname: Redaelli
authors.forename: G
authors.initials: G
authors.lastname: Colloredo
authors.forename: E
authors.initials: E
authors.lastname: Minola
authors.forename: C
authors.initials: C
authors.lastname: Donada
authors.forename: A
authors.initials: A
authors.lastname: Picciotto
authors.forename: P
authors.initials: P
authors.lastname: Riboli
authors.forename: P
authors.initials: P
authors.lastname: Del Poggio
authors.forename: G
authors.initials: G
authors.lastname: Rinaldi
authors.forename: B
authors.initials: B
authors.lastname: Paris
authors.forename: G
authors.initials: G
authors.lastname: Fornaciari
authors.forename: M
authors.initials: M
authors.lastname: Giusti
authors.forename: R
authors.initials: R
authors.lastname: Marin
authors.forename: R
authors.initials: R
authors.lastname: Morales
authors.forename: A
authors.initials: A
authors.lastname: Sangiovanni
authors.forename: G
authors.initials: G
authors.lastname: Belloni
authors.forename: M
authors.initials: M
authors.lastname: Pozzi
authors.forename: G
authors.initials: G
authors.lastname: Poli
authors.forename: N
authors.initials: N
authors.lastname: Mascoli
authors.forename: C
authors.initials: C
authors.lastname: Corradi
authors.forename: P
authors.initials: P
authors.lastname: Pioltelli
authors.forename: A
authors.initials: A
authors.lastname: Scalori
authors.forename: G
authors.initials: G
authors.lastname: Mancia
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000998:Antiviral Agents / Q000627:therapeutic use; D001706:Biopsy; D015331:Cohort Studies; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000188:drug therapy / Q000473:pathology*; D006801:Humans; D007372:Interferons / Q000627:therapeutic use; D008099:Liver / Q000473:pathology; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011379:Prognosis; D012189:Retrospective Studies; D012307:Risk Factors; D016019:Survival Analysis; D016896:Treatment Outcome
chemical_list: D000998:Antiviral Agents; D007372:Interferons