Steatosis accelerates the progression of liver damage of chronic hepatitisC patients and correlates with specific HCV genotype and visceral obesity

Citation
Le. Adinolfi et al., Steatosis accelerates the progression of liver damage of chronic hepatitisC patients and correlates with specific HCV genotype and visceral obesity, HEPATOLOGY, 33(6), 2001, pp. 1358-1364
Citations number
36
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATOLOGY
ISSN journal
02709139 → ACNP
Volume
33
Issue
6
Year of publication
2001
Pages
1358 - 1364
Database
ISI
SICI code
0270-9139(200106)33:6<1358:SATPOL>2.0.ZU;2-A
Abstract
The role of steatosis in the progression of liver damage in chronic hepatit is C (CHC) was studied. Enrolled were 180 consecutive liver biopsy-proven C HC patients and 41 additional subjects with a known duration of infection. We evaluated the histological activity index (HAI), grade of fibrosis and s teatosis, body mass index (BMI; kg/m(2)), distribution of body fat, HCV gen otype, and levels of HCV RNA. Eighty six (48%) patients showed steatosis, a nd a higher prevalence was observed in genotype 3a infection (P < .01), A c orrelation between the grade of steatosis and fibrosis was observed (P < .0 01). Fibrosis was also associated with age (P < .001). After adjusting for age, the association between steatosis and fibrosis remained significant. T he grade of steatosis also correlated with the HAI (P < .007) with a signif icant increase in periportal necrosis. No relation was found between steato sis and age, gender, iron storage, or levels of HCV RNA. Patients with a hi gh grade of steatosis (>30%) showed higher serum levels of gamma -GT and AL T (P < .001), Overall, steatosis was not significantly associated to BMI. A nalysis by single genotype showed a significant association between the gra de of steatosis and BMI in type 1 infection r = .689; P < .001) and with le vels of HCV RNA in type 3a infection r = .786; P <.001). Visceral fat distr ibution rather than BMI proved to be associated with steatosis (P < .001). Data obtained from patients with a known date of infection confirmed that s teatosis grades 3-4 were associated with a higher annual rate of fibrosis p rogression, and showed that alcohol and steatosis act together in increasin g fibrosis (P < .05), Our data indicate that steatosis is an important cofa ctor in increasing liver necroinflammatory activity and in accelerating fib rosis in CHC. Visceral obesity and genotype 3a play a role in the developme nt of steatosis.