Lipid Profiles and Hepatitis C Viral Markers in HCV-Infected Thalassemic Patients
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Background/Aims: The distribution of blood lipids, glucose and their determinants in thalassemic patients with chronic hepatitis C virus (HCV) infection has rarely been investigated. Thus, we aimed to investigate the relationship between both liver histologic findings and viral markers and serum lipids in thalassemic patients chronically infected with HCV. Methods: We enrolled 280 polytransfused thalassemic patients with chronic hepatitis C. HCV viral load was determined using the Amplicor test. Genotyping was performed using genotype specific primers. Fasting serum lipid, glucose, ferritin and liver function enzyme concentrations were measured. A modified Knodell scoring system was used to stage liver fibrosis and to grade necroinflammatory activity. Perls’ staining was used to assess hepatic siderosis. Results: Just one subject had total cholesterol >200 mg/dL, and 7% had triglycerides >150 mg/dL. The mean high-density lipoprotein cholesterol (HDL-C) and glucose levels were 37 and 104 (97-111) mg/dL, respectively. Viral markers, liver histological findings and aminotransferase activity were not associated with serum lipid levels. Serum triglycerides, total cholesterol and ferritin were independent risk factors for impaired glucose tolerance or diabetes in these patients. Conclusions: The majority of the patients had blood lipid levels (with the exception of HDL) within the defined normal range; viral and liver histological factors do not appear to play a significant role in changing the levels of serum lipids or glucose in these patients.
Abstract
Background/Aims: The distribution of blood lipids, glucose and their determinants in thalassemic patients with chronic hepatitis C virus (HCV) infection has rarely been investigated. Thus, we aimed to investigate the relationship between both liver histologic findings and viral markers and serum lipids in thalassemic patients chronically infected with HCV. Methods: We enrolled 280 polytransfused thalassemic patients with chronic hepatitis C. HCV viral load was determined using the Amplicor test. Genotyping was performed using genotype specific primers. Fasting serum lipid, glucose, ferritin and liver function enzyme concentrations were measured. A modified Knodell scoring system was used to stage liver fibrosis and to grade necroinflammatory activity. Perls’ staining was used to assess hepatic siderosis. Results: Just one subject had total cholesterol >200 mg/dL, and 7% had triglycerides >150 mg/dL. The mean high-density lipoprotein cholesterol (HDL-C) and glucose levels were 37 and 104 (97-111) mg/dL, respectively. Viral markers, liver histological findings and aminotransferase activity were not associated with serum lipid levels. Serum triglycerides, total cholesterol and ferritin were independent risk factors for impaired glucose tolerance or diabetes in these patients. Conclusions: The majority of the patients had blood lipid levels (with the exception of HDL) within the defined normal range; viral and liver histological factors do not appear to play a significant role in changing the levels of serum lipids or glucose in these patients.
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