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
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.