Journal
GUT
Volume 61, Issue 1, Pages 128-134Publisher
BMJ PUBLISHING GROUP
DOI: 10.1136/gut.2010.236158
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Funding
- Human Genome Sciences Inc, Rockville, Maryland, USA
- Novartis Pharma AG, Basel, Switzerland
- HGS
- Novartis
- Human Genome Sciences Inc
- Duke Clinical Research Institute
- National Health and Medical Research Council of Australia
- Gastroenterology Society of Australia
- Human Genome Sciences (HGS)
- Hoffman-LaRoche Inc, Nutley, New Jersey
- Roche
- NATIONAL CANCER INSTITUTE [K24CA139570] Funding Source: NIH RePORTER
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Objectives Genotype-specific associations between hepatitis C virus (HCV) and insulin resistance (IR) have been described, but a causal relationship remains unclear. This study investigated the association between a sustained virological response (SVR) and IR after chronic HCV therapy. Methods 2255 treatment-naive patients with chronic HCV genotype 1 or 2/3 were enrolled in two phase 3 trials of albinterferon alpha-2b versus pegylated interferon alpha-2a for 48 or 24 weeks, respectively. IR was measured before treatment and 12 weeks after treatment using homeostasis model assessment (HOMA)-IR. Results Paired HOMA-IR measurements were available in 1038 non-diabetic patients (497 with genotype 1; 541 with genotype 2/3). At baseline the prevalence of HOMA-IR >3 was greater in patients with genotype 1 than 2/3 (33% vs 27%; p=0.048). There was a significant reduction in the prevalence of IR in patients with genotype 1 achieving SVR (delta 10%; p<0.001), but not in genotype 1 non-responders or those with genotype 2/3. Multivariate analysis indicated that SVR was associated with a significant reduction in mean HOMA-IR in patients with genotype 1 (p=0.004), but not in those with genotype 2/3, which was independent of body mass index, alanine transaminase, gamma-glutamyl transpeptidase and lipid level changes. Conclusions SVR is associated with a reduction in HOMA-IR in patients with HCV genotype 1 but not in those with genotype 2/3. Genotype 1 may have a direct effect on the development of IR, independent of host metabolic factors, and may be partially reversed by viral eradication.
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