Hepatocellular fat accumulation and low serum cholesterol in patients infected with HCV-3a.

OBJECTIVES: The aim of this study was to prospectively investigate the prevalence of hepatic steatosis in chronic hepatitis C patients with respect to viral genotype, hepatic iron concentration, total body iron, body mass index, and serum lipid parameters. Furthermore, the effect of hepatitis C virus (HCV) eradication by antiviral therapy on serum cholesterol levels was studied.
METHODS: Hepatocellular fat and hepatic iron were determined in liver biopsies obtained from 137 interferon-naïve patients with chronic hepatitis C (100 men, 37 women, mean age 40.8 +/- 10.7 yr) enrolled in two prospective clinical trials of interferon/ribavirin therapy. Body mass index and fasting cholesterol levels were determined at baseline, during, and after therapy.
RESULTS: Marked steatosis (>20% of fat-containing hepatocytes) was found in 74.5% of patients infected with HCV-3a compared with 17.9% in HCV-1 and 21.7% in HCV-4-infected patients (p < 0.01). Steatosis in HCV-3a-infected patients did not correlate with the body mass index, hepatic iron content, ferritin, or transferrin saturation. At baseline, serum cholesterol was lower in patients infected with HCV-3a (147 +/- 42 mg/dl; p < 0.01) compared with HCV-1 (188 +/- 36) or HCV-4 (172 +/- 35). In contrast to HCV-1- or HCV-4-infected patients, serum cholesterol increased in HCV-3a virological responders at the end of treatment and 6 months after therapy (baseline 146 +/- 38, end of treatment 166 +/- 29, p < 0.05, sustained virological response 200 +/- 34, p < 0.01). However, serum cholesterol remained unchanged in HCV-3a nonresponders.
CONCLUSIONS: Our data suggest that, in addition to inducing steatosis, HCV-3a lowers serum cholesterol. This metabolic effect is fully reversible after successful HCV-3a eradication. This unique property is not shared by other HCV genotypes.