The association between hepatitis C infection (HCV) and type 2 diabetes was first recognized in 1994, when multiple studies noted an increased prevalence of type 2 diabetes in patients infected with HCV compared to patients with hepatitis B infection (HBV) or those with chronic liver disease from other causes. It remains unclear how HCV impairs glucose metabolism, and therefore how to combat it however, a case study by the University of Ottawa published in The American Journal of Case Reports details a patient who was able to reverse his glucose abnormalities by eradicating his HCV infection. While previous cases have reported improvements in glucose control with HCV treatment, these effects were limited to just the treatment phase; this is the first case to show complete diabetes remission beyond the treatment phase.
The patient was a 49-year-old man with no previous history of diabetes, but who had polyuria, polydipsia, fasting blood sugar of 18mmol/L, and an HbA1c of 10%. He had obtained HCV through blood transfusion and he also had non-alcoholic steatohepatitis and early-stage cirrhosis. His previous treatment for HCV involved pegylated-interferon/ribavirin (peg-IFN/rib) but this did not achieve a sustained virological response (SVR). Upon referral to Endocrinology he was diagnosed with type 2 diabetes and began taking diabetes medications (metformin and a sulfonylurea).
His HbA1c was down to 7.7% within a month of starting diabetes treatment and his blood sugars stayed between 5–7mmol/L. Maintaining this treatment regime for the next two years the patient had HbA1c of between 4.6 and 8.6%. He was then retreated with peg-IFN/rib plus boceprevir (an HCV protease inhibitor) for a 48-week period, during which time no changes were made to his diabetes medications. His glucose control improved in tandem with the antiviral response to his HCV therapy. This time his HCV treatment was successful, and he achieved a sustained virological response. After a year of completing the antiviral therapy his diabetes medications were no longer necessary. More than two years after completion of HCV antiviral treatment, the patient remains aviremic and has maintained an HbA1c of 5.8%, without any diabetes medication.
Studies estimate the prevalence of type 2 diabetes among HCV-infected patients to vary between 14.5% and 33%. Just how HCV impairs insulin sensitivity is likely multifaceted, as HCV is constrained to the liver but insulin sensitivity is impaired in the liver and also the periphery. This case study demonstrates the need for close glucose monitoring during HCV treatment since dosage adjustments of diabetes medications may be necessary in order to avoid hypoglycemia. A potentially greater discovery of the study is the possible reversibility of impaired glucose metabolism with viral eradication of HCV.
Considering how little is known, the findings in this study suggest further research into the causative link between insulin resistance and HCV are needed.
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