Insulin resistance predicts sustained virological response to treatment of chronic hepatitis C independently of the IL28b rs12979860 polymorphism
Article first published online: 5 NOV 2012
© 2012 Blackwell Publishing Ltd
Alimentary Pharmacology & Therapeutics
Volume 37, Issue 1, pages 74–80, January 2013
How to Cite
del Campo, J. A., Ampuero, J., Rojas, L., Conde, M., Rojas, Á., Maraver, M., Millán, R., García-Valdecasas, M., García-Lozano, J. R., González-Escribano, M. F. and Romero-Gómez, M. (2013), Insulin resistance predicts sustained virological response to treatment of chronic hepatitis C independently of the IL28b rs12979860 polymorphism. Alimentary Pharmacology & Therapeutics, 37: 74–80. doi: 10.1111/apt.12113
- Issue published online: 4 DEC 2012
- Article first published online: 5 NOV 2012
- Manuscript Accepted: 9 OCT 2012
- Manuscript Revised: 27 SEP 2012
- Manuscript Revised: 22 JUL 2012
- Manuscript Received: 3 JUL 2012
- Government of Andalusia Health Department. Grant Number: 448/09
- Instituto de Salud Carlos III. Grant Number: 10/00611
Insulin resistance has been strongly associated with the attainment of sustained viral response (SVR) in hepatitis C patients.
To determine, in a cohort of Spanish patients with chronic hepatitis C treated with peginterferon plus ribavirin (P+R), whether insulin resistance predicts SVR independently of interleukin-28B rs12979860 polymorphism.
Insulin resistance was measured as [HOMA-IR = Insulin (IU/mL)*glucose (mmol/L)/22.5]. Genotype, viral load and histological fibrosis using Scheuer score were also measured. Binary logistic regression analysis was used for statistical purposes.
In a cohort of 240 patients [78% genotype 1, 24% showing advanced fibrosis, 71% high viral load (≥800 000 IU/mL), 31% IL28b genotype CC and 50% with HOMA >2] treated with P+R, 126 (53%) reached SVR. HOMA-IR index (HOMA <2: 63% vs. HOMA >2: 42%; P = 0.001 and IL28b (genotype CC: 68% vs. genotype CT/TT: 45%; P = 0.002) were significantly associated with SVR. In multivariable logistic regression analysis in the overall cohort, variables independently associated were: viral genotype OR: 0.29 (95% CI: 0.11–0.78), P = 0.01; fibrosis OR: 1.62 (95% CI: 1.22–2.16), P = 0.001; HOMA-IR OR: 1.22 (95% CI: 1.02–1.47), P = 0.03; and IL28B genotype OR: 2.43 (95% CI: 1.45–4.07), P = 0.001. The analyses also showed that degree of steatosis, HOMA-IR >2, mild fibrosis and IL28B CC genotype were significantly related to SVR in patients infected with HCV genotypes 1&4, but not in those with genotypes 2&3. No differences were seen in glucose, insulin level or HOMA-IR index segregated according to IL28B genotypes.
Our results suggest that insulin resistance, fibrosis stage and IL28B polymorphisms were independent variables associated with sustained viral response.