Hepatitis C virus–associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis

A relationship between chronic hepatitis C virus (HCV) infection and lipid metabolism has recently been suggested. The aim of this study was to determine the correlation between lipid profile and virology, histologic lesions, and response to α interferon therapy in noncirrhotic, nondiabetic patients with hepatitis C. A total of 109 consecutive untreated chronic hepatitis C patients were studied to assess the following: 1) the effects of HCV genotype, viral load, steatosis, hepatic fibrosis, and body mass index (BMI) on lipid profile; and 2) whether lipid parameters could predict response to antiviral therapy. The control group showed a significantly higher apolipoprotein B (apoB) concentration compared with patients with chronic hepatitis C. Hypobetalipoproteinemia (apo B 5% ( p < 0.001), low body mass index ( p < 0.001), and high HCV viral load ( p < 0.014). No correlation was found in the 76 treated patients between apo B and response to interferon therapy. In chronic HCV patients, hypobetalipoproteinemia occurs already in the early stages of HCV infection before the development of liver cirrhosis. The correlation between apo B levels and HCV viral load seems to confirm the interaction between hepatitis C infection and β-lipoprotein metabolism.