Hepatitis C Virus–Associated Hypobetalipoproteinemia Is Correlated With Plasma Viral Load, Steatosis, and Liver Fibrosis

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Abstract
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 p = 0.0002). Levels of apo B were negatively correlated with steatosis and HCV viral load (r= − 0.22; p = 0.03). This last correlation was strong for non-1 genotype and genotype 3 (r= − 0.48; p = 0.0005, and r= − 0.47; p = 0.007, respectively) but was not found in genotype 1. In multivariate analysis, low apo B concentration was significantly associated with fibrosis grade 2 or 3 versus grade 0 or 1 (p < 0.001), steatosis >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.