A team from Naples, Italy, studied the role of steatosis in the progression of liver damage in chronic hepatitis C (CHC).
180 consecutive liver biopsy-proven CHC patients, and 41 additional subjects with a known duration of infection, were enrolled.
Histological activity index (HAI) and grade of fibrosis and steatosis were evaluated. Body mass index (BMI; kg/m2), distribution of body fat, HCV genotype, and levels of HCV RNA were also assessed.
86 (48%) patients were found to show steatosis. A higher prevalence was observed in genotype 3a infection.
A correlation between the grade of steatosis and fibrosis was observed.
Fibrosis was also associated with age. After adjusting for age, the association between steatosis and fibrosis remained significant.
In addition, the grade of steatosis correlated with the HAI, with a significant increase in periportal necrosis.
Steatosis is an important cofactor . . . in accelerating fibrosis in chronic hepatitis C
|Professor Luigi E. Adinolfi|
The researchers found no relation between steatosis and age, gender, iron storage, or levels of HCV RNA.
Patients with a high grade of steatosis (more than 30%) showed higher serum levels of gamma-GT and ALT.
Overall, steatosis was not significantly associated to BMI. However, analysis by single genotype showed a significant association between the grade of steatosis and BMI in Type 1 infection and with levels of HCV RNA in Type 3a infection.
Visceral fat distribution, rather than BMI, proved to be associated with steatosis.
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. They also showed that alcohol and steatosis act together in increasing fibrosis.
Professor Luigi E. Adinolfi, of the Second University of Naples, concluded on behalf of the group, "Our data indicate that steatosis is an important cofactor in increasing liver necroinflammatory activity and in accelerating fibrosis in chronic hepatitis C.
"Visceral obesity and genotype 3a play a role in the development of steatosis."