Risk factors for the development of diabetes mellitus in chronic hepatitis C virus genotype 4 infection
Article first published online: 20 AUG 2008
© 2008 The Authors. Journal compilation © 2008 Journal of Gastroenterology and Hepatology Foundation and Blackwell Publishing Asia Pty Ltd
Journal of Gastroenterology and Hepatology
Volume 24, Issue 1, pages 42–48, January 2009
How to Cite
Chehadeh, W., Abdella, N., Ben-Nakhi, A., Al-Arouj, M. and Al-Nakib, W. (2009), Risk factors for the development of diabetes mellitus in chronic hepatitis C virus genotype 4 infection. Journal of Gastroenterology and Hepatology, 24: 42–48. doi: 10.1111/j.1440-1746.2008.05503.x
- Issue published online: 19 JAN 2009
- Article first published online: 20 AUG 2008
- Accepted for publication 16 April 2008.
- hepatitis C genotype 4;
- risk factors;
- sustained virological response;
- type 2 diabetes;
- viral load
Background and Aim: A high occurrence of type 2 diabetes (T2D) in patients with chronic hepatitis C virus (HCV) infection has been reported in Kuwait and other countries. However, HCV genotype 4 has been underrepresented in all previous studies. Our aim was to investigate the viral and host risk factors associated with the development of T2D in patients with chronic hepatitis C genotype 4 infection in the absence of liver fibrosis and steatosis.
Methods: The study population consisted of 181 HCV-positive patients and 170 control HCV-negative patients with T2D.
Results: The prevalence of HCV-patients with T2D was 39.8%. There was no significant association of T2D with gender, nationality, obesity, HCV viral load, or antiviral therapy. Older age (≥ 50 years) and family history of diabetes were the only independent risk factor for T2D in HCV patients. However, the median age and the prevalence of obesity in HCV-positive patients with T2D were significantly lower than those in diabetic HCV-negative patients. By following-up HCV-patients receiving antiviral drugs, a significant decrease of fasting plasma glucose and glycosylated hemoglobin levels was observed in diabetic patients who achieved a sustained viral response (SVR).
Conclusions: The risk factors associated with the development of T2D in the general population cannot alone account for the high prevalence of T2D obtained in chronic HCV genotype 4 infection. In the absence of liver fibrosis and steatosis, the improvement in glycemic control obtained in SVR patients may imply direct involvement of HCV in the development of T2D.