All authors contributed equally to this article.
Use of HOMA-IR in hepatitis C
Version of Record online: 25 MAY 2011
© 2011 Blackwell Publishing Ltd
Journal of Viral Hepatitis
Volume 18, Issue 10, pages 675–684, October 2011
How to Cite
Eslam, M., Kawaguchi, T., Del Campo, J. A., Sata, M., Abo-Elneen Khattab, M. and Romero-Gomez, M. (2011), Use of HOMA-IR in hepatitis C. Journal of Viral Hepatitis, 18: 675–684. doi: 10.1111/j.1365-2893.2011.01474.x
- Issue online: 14 SEP 2011
- Version of Record online: 25 MAY 2011
- Received December 2010; accepted for publication March 2011
- hepatitis C virus;
- hyperinsulinaemic euglycaemic glucose clamp;
- insulin resistance
Summary. Chronic infection with hepatitis C virus (HCV) can induce insulin resistance (IR) in a genotype-dependent manner and contributes to steatosis, progression of fibrosis and resistance to interferon plus ribavirin therapy. Our understanding of HCV-induced IR has improved considerably over the years, but certain aspects concerning its evaluation still remain elusive to clinical researchers. One of the most important issues is elucidating the ideal method for assessment of IR in the setting of hepatitis C. The hyperinsulinaemic euglycaemic clamp is the gold standard method for determining insulin sensitivity, but is impractical as it is labour intensive and time-consuming. To date, all human studies except for four where IR was evaluated in the HCV setting, an estimation of IR has been used rather than direct measurements of insulin-mediated glucose uptake. The most commonly used estimation in the HCV population is the homeostasis model assessment of insulin resistance (HOMA-IR) which is calculated from a single measurement of fasting insulin and glucose. In this article, we review the use and reporting of HOMA in the literature and provide guidance on its appropriate as well as inappropriate use in the hepatitis setting.