title: Steatosis accelerates the progression of liver damage of chronic hepatitis C patients and correlates with specific HCV genotype and visceral obesity.
abstract: The role of steatosis in the progression of liver damage in chronic hepatitis C (CHC) was studied. Enrolled were 180 consecutive liver biopsy-proven CHC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and steatosis, body mass index (BMI; kg/m(2)), distribution of body fat, HCV genotype, and levels of HCV RNA. Eighty six (48%) patients showed steatosis, and a higher prevalence was observed in genotype 3a infection (P <.01). A correlation between the grade of steatosis and fibrosis was observed (P <.001). Fibrosis was also associated with age (P <.001). After adjusting for age, the association between steatosis and fibrosis remained significant. The grade of steatosis also correlated with the HAI (P <.007) with a significant increase in periportal necrosis. No relation was found between steatosis and age, gender, iron storage, or levels of HCV RNA. Patients with a high grade of steatosis (>30%) showed higher serum levels of gamma-GT and ALT (P <.001). Overall, steatosis was not significantly associated to BMI. Analysis by single genotype showed a significant association between the grade of steatosis and BMI in type 1 infection r =.689; P <.001) and with levels of HCV RNA in type 3a infection r =.786; P <.001). Visceral fat distribution rather than BMI proved to be associated with steatosis (P <.001). Data obtained from patients with a known date of infection confirmed that steatosis grades 3-4 were associated with a higher annual rate of fibrosis progression, and showed that alcohol and steatosis act together in increasing fibrosis (P <.05). Our data indicate that steatosis is an important cofactor in increasing liver necroinflammatory activity and in accelerating fibrosis in CHC. Visceral obesity and genotype 3a play a role in the development of steatosis.
authors.affiliation: Internal Medicine & Hepatology, Second University of Naples, Naples, Italy. luigielo.adinolfi@unina2.it
authors.forename: L E
authors.initials: LE
authors.lastname: Adinolfi
authors.forename: M
authors.initials: M
authors.lastname: Gambardella
authors.forename: A
authors.initials: A
authors.lastname: Andreana
authors.forename: M F
authors.initials: MF
authors.lastname: Tripodi
authors.forename: R
authors.initials: R
authors.lastname: Utili
authors.forename: G
authors.initials: G
authors.lastname: Ruggiero
mesh_terms: D000328:Adult; D000368:Aged; D015331:Cohort Studies; D018450:Disease Progression; D005234:Fatty Liver / Q000150:complications* / Q000503:physiopathology; D005260:Female; D005838:Genotype; D016174:Hepacivirus / Q000235:genetics*; D019698:Hepatitis C, Chronic / Q000150:complications* / Q000473:pathology* / Q000503:physiopathology / Q000821:virology; D006801:Humans; D008099:Liver / Q000473:pathology* / Q000503:physiopathology; D008111:Liver Function Tests; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000150:complications* / Q000473:pathology; D013997:Time Factors; D014781:Viscera / Q000473:pathology