We report on a patient whose type 2 diabetes resolved following interferon-α (IFN-α) therapy for hepatitis C virus (HCV). A 57-years-old man, presented with fatigue, polyuria and polydipsia. He was newly diagnosed with type 2 diabetes. During the hospital day, he was also diagnosed with chronic hepatitis. Serological studies for chronic hepatitis demonstrated presence of hepatitis C, type 2a/2c genotype. He was started on subcutaneous insulin and IFN-α. After 24 weeks of treatment of IFN-α, HCV polymerase chain reaction was negative. And diabetes resolved despite an increase in his body weight. A number of papers have described associations between IFN-α therapy and the precipitation of diabetic ketoacidosis as the presenting feature of new-onset diabetes. Our case shows a resolution of diabetes after IFN-α therapy for chronic hepatitis C. HCV mainly affects the liver, but also several tissues outside the liver have been reported to be involved, resulting in a wide spectrum of extrahepatic manifestations. It has been hypothesized that diabetes also could be one of these extrahepatic conditions attributable to HCV infection. Previous HCV infection markedly increased the prevalence of type 2 diabetes, regardless of the presence of liver cirrhosis. Non-diabetic HCV patients have insulin resistance and specific defects in the insulin-signaling pathway. The specific mechanisms by which HCV lead to type 2 diabetes are not fully understood, but it seems that an increase of insulin resistance associated with both steatosis and the overproduction of pro-inflammatory cytokine could play a crucial role. Although it is unclear whether the resolution of diabetes in this case occurred as an effect of IFN-α or as a result of becoming HCV RNA negative, it has suggested a great deal about the role of IFN-α and HCV infection in the pathogenesis of diabetes.
Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.
Funding: This research did not receive any specific grant from any funding agency in the public, commercial or not-for-profit sector.
05 - 09 May 2012
European Society of Endocrinology