title: HCV genotype 3 is associated with a higher hepatocellular carcinoma incidence in patients with ongoing viral C cirrhosis.
abstract: Liver steatosis is a main histopathological feature of Hepatitis C (HCV) infection because of genotype 3. Steatosis and/or mechanisms underlying steatogenesis can contribute to hepatocarcinogenesis. The aim of this retrospective study was to assess the impact of infection with HCV genotype 3 on hepatocellular carcinoma (HCC) occurrence in patients with ongoing HCV cirrhosis. Three hundred and fifty-three consecutive patients (193 men, mean age 58 ± 13 years), with histologically proven HCV cirrhosis and persistent viral replication prospectively followed and screened for HCC between 1994 and 2007. Log-rank test and Cox model were used to compare the actuarial incidence of HCC between genotype subgroups. The patients infected with a genotype 3 (n = 25) as compared with those infected with other genotypes (n = 328) had a lower prothrombin activity [78 (interquartile range 60-85) vs 84 (71-195) %, P = 0.03] and higher rate of alcohol abuse (48%vs 29%, P = 0.046). During a median follow-up of 5.54 years [2.9-8.6], 11/25 patients (44%) and 87/328 patients (26%) with a genotype 3 and non-3 genotype, respectively, develop a HCC. HCC incidences were significantly different among the genotype subgroups (P = 0.001). The 5-year occurrence rate of HCC was 34% (95% CI, 1.3-6.3) and 17% (95% CI, 5.7-9.2) in genotype 3 and non-3 genotype groups, respectively (P = 0.002). In multivariate analysis, infection with a genotype 3 was independently associated with an increased risk of HCC occurrence [hazard ratio 3.54 (95% CI, 1.84-6.81), P = 0.0002], even after adjustment for prothrombin activity and alcohol abuse [3.58 (1.80-7.13); P = 0.003]. For patients with HCV cirrhosis and ongoing infection, infection with genotype 3 is independently associated with an increased risk of HCC development.
authors.affiliation: Department of Hepatogastroenterology, Hôpital Jean Verdier (Assistance Publique-Hôpitaux de Paris), Bondy, France. gisele.nkontchou@jvr.aphp
authors.forename: G
authors.initials: G
authors.lastname: Nkontchou
authors.forename: M
authors.initials: M
authors.lastname: Ziol
authors.forename: M
authors.initials: M
authors.lastname: Aout
authors.forename: M
authors.initials: M
authors.lastname: Lhabadie
authors.forename: Y
authors.initials: Y
authors.lastname: Baazia
authors.forename: A
authors.initials: A
authors.lastname: Mahmoudi
authors.forename: D
authors.initials: D
authors.lastname: Roulot
authors.forename: N
authors.initials: N
authors.lastname: Ganne-Carrie
authors.forename: V
authors.initials: V
authors.lastname: Grando-Lemaire
authors.forename: J-C
authors.initials: JC
authors.lastname: Trinchet
authors.forename: E
authors.initials: E
authors.lastname: Gordien
authors.forename: E
authors.initials: E
authors.lastname: Vicaut
authors.forename: I
authors.initials: I
authors.lastname: Baghad
authors.forename: M
authors.initials: M
authors.lastname: Beaugrand
mesh_terms: D000368:Aged; D006528:Carcinoma, Hepatocellular / Q000453:epidemiology*; D005234:Fatty Liver / Q000150:complications / Q000473:pathology / Q000821:virology; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000145:classification* / Q000235:genetics / Q000302:isolation & purification / Q000472:pathogenicity*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000473:pathology / Q000821:virology*; D006801:Humans; D015994:Incidence; D008103:Liver Cirrhosis / Q000150:complications* / Q000473:pathology / Q000821:virology*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies