Published online Jan 18, 2016. doi: 10.4254/wjh.v8.i2.131
Peer-review started: July 11, 2015
First decision: September 16, 2015
Revised: December 10, 2015
Accepted: December 29, 2015
Article in press: January 4, 2016
Published online: January 18, 2016
Processing time: 192 Days and 12.5 Hours
Chronic hepatitis C virus (HCV) infection has been shown to be linked to a higher prevalence of type 2 diabetes compared with the general population or with patients with chronic hepatitis B infection and diabetes is the most common extra-hepatic manifestation of HCV. The HCV-diabetes association is due to insulin resistance (IR) that occurs early in the course of the disease even in patients without or with minimal fibrosis. The mechanisms for HCV-induced IR are only partly understood and include a direct inhibitory effect of HCV on insulin signaling pathway. IR in chronic HCV results in an increased progression rate of hepatic fibrosis, cirrhosis and hepatocellular carcinoma. Some but not all studies found that IR reduces the response rate to interferon/ribavirin therapy. Whether IR affects the response to the new direct-acting antiviral treatments is still unknown.
Core tip: Chronic hepatitis C virus (HCV) infection is associated with a higher prevalence of diabetes as compared to either the general population or patients with chronic hepatitis B infections. HCV hepatitis is linked to insulin resistance (IR) early in the disease course, mediated partly by direct inhibitory effect of the viral proteins on insulin signaling. The presence of IR is associated with an increased rate of disease progression to fibrosis, cirrhosis and hepatocellular carcinoma. Interferon and ribavirin treatment of HCV hepatitis may be less successful in the presence of IR. The effect of IR on the new direct-acting antiviral treatment is unclear.