51. Long-term reversal of hypocholesterolaemia in patients with chronic hepatitis C is related to sustained viral response and viral genotype.
- Author
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Fernández-Rodríguez CM, López-Serrano P, Alonso S, Gutiérrez ML, Lledó JL, Pérez-Calle JL, Temiño R, Cacho G, Nevado M, Casas ML, Gasalla JM, and Bonet B
- Subjects
- Cholesterol deficiency, Fatty Liver etiology, Female, Genotype, Humans, Male, Middle Aged, C-Peptide metabolism, Cholesterol blood, Dyslipidemias virology, Hepatitis C, Chronic complications, Hepatitis C, Chronic genetics, Leptin metabolism
- Abstract
Background: Genotype-3 of hepatitis C virus (HCV) has been associated with serum lipid changes (reversible with sustained viral response) and liver steatosis., Aim: To characterize the relationships among hepatic steatosis, cholesterol and sustained viral response in these patients., Methods: Patients (n = 215) with chronic hepatitis C (157 with genotype-1 of HCV) had age, body mass index, gender, alcohol intake, glycaemia, serum lipids, transaminases, grade and stage (METAVIR and Scheuer), degree of liver steatosis, sustained viral response, insulinaemia, leptinaemia, beta-hydroxybutyrate and glycerol measured, and were compared with 32 hepatitis B virus (HBV)-infected subjects., Results: Genotype-3 of HCV patients had age-adjusted hypocholesterolaemia and more frequent hepatic steatosis (P < 0.001). Steatosis was inversely correlated with serum cholesterol (P < 0.01) and directly with viral load (P < 0.03). In patients with genotype-3 of HCV and sustained viral response, serum cholesterol increased from 138 (95% CI: 120-151) to 180 mg/dL (95% CI: 171-199) 12 months after treatment conclusion (P < 0.0001). By contrast, cholesterol values were unchanged in genotype-3 of HCV non-responders and in patients with genotype-1 of HCV regardless of response. Rising cholesterol in sustained viral response did not parallel the changes in beta-hydroxybutyrate., Conclusions: Besides causing hepatic steatosis, genotype-3 specifically decreases serum cholesterol. This interference with the metabolic lipid pathway is related to viral load, is reversed with sustained viral response, and seems unrelated to mitochondrial dysfunction.
- Published
- 2006
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