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HCV Eradication Lowers Glucose Levels in Veterans With Diabetes

by U.S. Medicine

December 15, 2017

PORTLAND, OR—Hepatitis C virus (HCV) infection is linked to diabetes and often worsens glycemic control in patients with diabetes.

A study published in Diabetes Care investigated whether eradication of HCV infection with direct-acting antiviral (DAAs) agents is associated with improved glycemic control in patients with diabetes.1

VA researchers from Portland, OR, and Seattle identified 2,435 patients with diabetes who underwent interferon-free and ribavirin-free DAA-based antiviral treatment for HCV in the national VA healthcare system. They tracked changes in average hemoglobin A1c (HbA1c) level and use of antidiabetic medications one year before and after antiviral treatment between patients who achieved sustained virologic response (SVR) and those who did not.

Results indicated that, among patients with elevated baseline HbA1c, the drop in HbA1c associated with antiviral treatment was greater in those who achieved SVR (0.98%) than in those with treatment failure (0.65%) for an adjusted mean difference of 0.34.

In addition, use of antidiabetic medications decreased more in patients who achieved SVR than in those who sustained treatment failure, especially for the use of insulin, which dropped significantly from 41.3% to 38% in patients achieving SVR compared with a slight increase from 49.8% to 51% in those who had treatment failure.

“DAA-based eradication of HCV is associated with improved glycemic control in patients with diabetes as evidenced by decreased mean HbA1c and decreased insulin use,” study authors concluded. “These endocrine benefits of SVR provide additional justification for considering antiviral treatment in all patients with diabetes.”

  1. Hum J, Jou JH, Green PK, Berry K, Lundblad J, Hettinger BD, Chang M, Ioannou GN. Improvement in Glycemic Control of Type 2 Diabetes After Successful Treatment of Hepatitis C Virus. Diabetes Care. 2017 Sep;40(9):1173-1180. doi: 10.2337/dc17-0485. Epub 2017 Jun 28. PubMed PMID: 28659309.

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