According to a recently published study (Gut 2005;54:1003–8), insulin resistance is a worsening factor in hepatitis C virus (HCV) related chronic hepatitis. There is much debate as to whether insulin resistance depends on hepatitis C virus, or vice versa, or whether it is an independent syndrome.

As insulin resistance is the link between obesity, metabolic alterations, and endothelial damage, it is a characteristic feature of the metabolic syndrome. Non-alcoholic steatohepatitis is a recently recognised entity associated with the metabolic syndrome. It frequently overlaps with HCV related chronic hepatitis, sharing some histological features (mainly steatosis).

The aim of our study was to verify the possibility of improving the rate of antiviral treatment response by ameliorating the metabolic syndrome.¹

Thirty two naïve patients with HCV related chronic hepatitis and metabolic syndrome (assessed using ATP III criteria), genotype 1, aged 44–68 years (16 males), were consecutively enrolled. The population was divided into two groups: 15 patients (group A) were on a strict low calorie diet for three months to achieve a 10% reduction in body mass index (BMI) before starting treatment, whereas 17 were on a free diet for the same period (group B).

All patients were offered standard combined antiviral therapy Peg-interferon alpha 2b 1.5 μg/kg body weight/weekly and ribavirin 1000–1200 µg/daily) for at least three months for non-responders (same virological load before and after) and for 12 months if responders or partial responders (decrease in HCV-RNA ⩾2 log 10). The results were as follows: homeostasis model of assessment (HOMA) in group A was different before and after weight reduction (4.86 (0.96) v 3.45 (0.66); p = 0.0018; paired t test), with 60% and 17.6% of responses in group A and B, respectively (p = 0.035; χ²). The flu-like-syndrome was present in eight patients in group A and in 13 patients in group B.

The low calorie diet was the only parameter differentiating the response rates to antiviral therapy. We speculate that by improving the metabolic syndrome, the decrease in BMI played a key role in reducing the metabolic cofactors and creating a better basis for a good antiviral response. The lower dosages encouraged better patient compliance to treatment.