Abstract
BackgroundThe hepatitis C virus (HCV) genotype-specific impacts on the host metabolic alterations remained inconclusive.MethodsA prospective study including 229 (118 genotype 1 (G1) and 111 G2) consecutive chronic HCV patients who had completed a course of anti-HCV treatment and underwent pre- and 24 weeks post-treatment surveys of metabolic profiles was conducted. Patients were stratified according to the therapeutic response, viral genotype and baseline insulin resistance (IR: homeostasis model assessments of IR (HOMA-IR) ≥2.5). Paired t-tests were used to compare the pre- and post-treatment variables.ResultsSignificant post-therapeutic increases in cholesterol, triglyceride, HDL, LDL, apolipoprotein A1 and apolipoprotein B were observed in patients with sustained virological response (SVR) but not in those without. Among those with SVR, post-therapeutic increases in HDL (p<0.001) and apolipoprotein A1 (p = 0.012) were only found in G2, whereas increased triglyceride/HDL (p = 0.01) ratios were only found in G1 patients. When stratified by baseline IR among those with SVR, a significant increase in post-treatment HDL (p = 0.019) and apolipoprotein A1 (p = 0.012) but a decrease in HOMA-IR (p = 0.04), C-peptide (p = 0.019) and hemoglobin A1c (p = 0.047) were found in patients with baseline IR; a significant increase in HOMA-IR (p = 0.002) was found in patients without baseline IR. The latter change was observed only in G1 (p = 0.01) but not G2 patients. Although the pre-treatment metabolic profiles of G1 and G2 patients were indifferent, G1 had higher post-treatment triglyceride/HDL ratios (p = 0.041) and triglyceride (p = 0.044) levels than G2 patients.ConclusionsG2 benefit more than G1 patients from viral clearance in metabolic alterations, particularly in those without baseline IR.
Highlights
The hepatitis C virus (HCV) is a human pathogen responsible for acute and chronic liver disease, infecting an estimated 130–170 million individuals worldwide [1]
Much of the HCV life cycle including the entry into naıve cells, infectivity, RNA replication, viral assembly and viral secretion closely associated with lipid metabolism [1,3]
The pre-treatment HCV RNA and HCV core Ag levels in genotype 1 (G1) patients were significantly higher than those of genotype 2 (G2) patients, while the sustained virological response (SVR) rate was higher in the G2 patients relative to the G1 patients
Summary
The hepatitis C virus (HCV) is a human pathogen responsible for acute and chronic liver disease, infecting an estimated 130–170 million individuals worldwide [1]. It is considered to cause metabolic alterations instead of being a viral infection. Much of the HCV life cycle including the entry into naıve cells, infectivity, RNA replication, viral assembly and viral secretion closely associated with lipid metabolism [1,3]. The combination of pegylated interferon (PegIFN)-a plus ribavirin has provided a ‘cure’ for a considerable proportion of patients with chronic hepatitis C (CHC), when most patients have the favorable interleukin-28B (IL-28B) genotype [5]. The hepatitis C virus (HCV) genotype-specific impacts on the host metabolic alterations remained inconclusive
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