Original contributionHepatitis C virus–associated hypobetalipoproteinemia is correlated with plasma viral load, steatosis, and liver fibrosis
Introduction
Interactions between chronic hepatitis C virus (HCV) infection and lipid metabolism have recently been suggested 1, 2, 3, 4, 5. Some studies have reported a higher prevalence of hypocholesterolemia and hypobetalipoproteinemia in HCV-infected patients compared with control groups 1, 2, 3. Although changed serum lipid and apolipoprotein composition is commonly found in patients with chronic liver disease of any etiology, the relationship between HCV and lipid metabolism seems to be more specific: binding of HCV particles to human high density lipoprotein (HDL), low density lipoprotein (LDL), and very low density lipoprotein (VLDL) has been described (4). Moreover the LDL receptors could permit the entry of HCV in hepatocytes 6, 7.
The pathogenesis of hypobetalipoproteinemia in patients with HCV is not well understood. Recently, an association between steatosis and hypobetalipoproteinemia has been demonstrated in HCV-infected patients (1); however, the influence of virologic parameters was not fully investigated. On the other hand, controversial results have been published on the relationship between lipid parameters and response to interferon therapy for chronic hepatitis C 1, 8, 9, 10. The significance of serum cholesterol and apolipoprotein levels as a predictor of response to interferon may be in connection with the decrease in serum cholesterol levels related to increasing severity of liver disease (9). This being so, the associations among serum lipid levels, liver histologic characteristics, virologic parameters, and response to interferon need to be explored.
The purpose of this study was to investigate the host and viral specific factors associated with the development of hypobetalipoproteinemia in patients with chronic hepatitis C.
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Study patients
A total of 109 untreated chronic hepatitis C patients were hospitalized for liver biopsy from January 1996 through December 1999. Collected data included age, sex, alcohol use, and family history of diabetes. Body mass index (BMI) was calculated as body weight in kilograms divided by the square of height in meters (kg/m2). Information regarding average alcohol intake in grams per day was assessed by interview. Patients consuming >60 g of alcohol daily were considered to be excessive drinkers.
Patient demographics and laboratory evaluation
The main clinical and laboratory data are summarized in Table 1. There were 70 men (mean age, 40.9 ± 11.8 yr) and 39 women (mean age, 49.2 ± 13.4 yr). The mean BMI was 23.3 ± 3.2 kg/m2 (range, 16.5–30.4); in men the BMI was 23.7 ± 3.2 kg/m2 and in women it was 22.5 ± 3.1 kg/m2. Age, BMI, and sex were not significantly different between patients and control subjects (Table 1). The control group showed a significantly higher apo B concentration compared with patients with chronic hepatitis C (
Discussion
The two major findings of this study of chronic noncirrhotic, nondiabetic HCV patients were 1) an association between hypobetalipoproteinemia and early stages of fibrosis and steatosis, and 2) a correlation between apo B level and HCV viral load.
Our findings are in agreement with the study of Serfaty et al. that have observed the high prevalence of hypobetalipoproteinemia in HCV-infected patients compared with healthy control subjects (1). These investigators observed that frequency of
Acknowledgements
This investigation was supported by the Centre Hospitalier Universitaire de Dijon (PHRC 2001).
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