Clinical

Insulin resistance, diabetes increase liver fibrosis in patients with genotype 1 HCV

Last Updated: 2008-06-25 14:18:40 -0400 (Reuters Health)

NEW YORK (Reuters Health) - Insulin resistance is a major determinant of advanced hepatic fibrosis in patients with chronic hepatitis C resulting from genotype 1 (G1-HCV), especially in the presence of severe necroinflammation, according to study findings published in the May issue of the American Journal of Gastroenterology.

"Metabolic factors may affect the course of chronic hepatitis C," Dr. Salvatore Petta, of the University of Palermo, Italy, and colleagues write. "Insulin resistance (IR) determines steatosis, but its direct role in affecting progression of hepatic fibrosis is less clear."

In the present study, the researchers examined whether increasing degrees of IR, up to overt diabetes, were associated with steatosis and higher stages of fibrosis in patients with G1-HCV.

Of the 201 patients, 55 (27%) had liver fibrosis of grade 3 or higher by the Scheuer score. Moderate/severe liver necroinflammation was observed in 72.7% of patients. Overall, 99 patients (49.3%) had histological evidence of steatosis.

The team reports that 95 of the subjects (47.3%) were not insulin resistant (group 1), 77 (38.3%) were insulin resistant without diabetes (group 2), and 29 (14.4%) were diabetic (group 3).

Results of multivariate analysis revealed an association between severe fibrosis (Scheuer score of 3 or greater) and prevalence of IR (odds ratio 2.69, p = 0.001) and high necroinflammatory activity (OR 2.99, p = 0.003).

Overall, 59% of patients in group 3 had severe fibrosis, compared to 30% of those in group 2 and 15% of those in group 1.

"Our study has conclusively demonstrated that IR, with or without diabetes, is a strong independent risk factor for fibrosis," Dr. Petta's team concludes. "Whether correcting IR by lifestyle modifications and/or the use of insulin-sensitizing drugs will modify the effect of IR on liver fibrosis remains to be demonstrated by appropriate trials."

Am J Gastroenterol 2008;103:1136-1144.