Research continues to clarify the association between metabolic factors and liver disease progression in people with chronic hepatitis C. In the May 2008 American Journal of Gastroenterology, S. Petta and colleagues assessed whether increasing degrees of insulin resistance – up to frank type 2 diabetes mellitus – were linked to liver steatosis (fat accumulation) and fibrosis in 201 Italian patients with HCV genotype 1. About half had normal insulin response, 38% had insulin resistance short of diabetes (HOMA-IR score > 2.7), and 14% were diabetic.

In a multivariate analysis, insulin resistance was among the factors that predicted advanced fibrosis (stage F3 or higher), independent of steatosis. Diabetic patients were twice as likely to have severe fibrosis as those with lesser degrees of insulin resistance (60 vs. 30%). In a related study reported in the June 2008 issue of Hepatology, B.J. Veldt and colleagues found that diabetes was also associated with a higher risk of hepatocellular carcinoma (HCC). The international research team analyzed 541 chronic hepatitis C patients with advanced fibrosis, 85 of whom (16%) had diabetes.

The prevalence of diabetes rose along with Ishak fibrosis scores, from 11% for patients with F4 fibrosis, to 13% for F5, to 19% for F6. During a median follow-up period of four years, 13% of diabetic patients developed HCC, compared with 6% of those without diabetes. At five years, the HCC incidence rates were 11% and 5%, respectively. “For patients with chronic hepatitis C and advanced cirrhosis,” the investigators concluded, “diabetes mellitus increases the risk of developing HCC.”

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