Relationship of hepatitis C virus infection with diabetes in the U.S. population

Authors

  • Constance E. Ruhl,

    Corresponding author
    1. Social & Scientific Systems, Inc., Silver Spring, MD
    • Address reprint requests to: Constance E. Ruhl, M.D., Ph.D., Social & Scientific Systems, Inc., 8757 Georgia Avenue, 12th Floor, Silver Spring, MD 20910. E-mail: cruhl@s-3.com; fax: 301-628-3201.

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  • Andy Menke,

    1. Social & Scientific Systems, Inc., Silver Spring, MD
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  • Catherine C. Cowie,

    1. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD
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  • James E. Everhart

    1. National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Department of Health and Human Services, Bethesda, MD
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  • Potential conflict of interest: Nothing to report.

  • This work was supported by a contract from the National Institute of Diabetes and Digestive and Kidney Diseases (HHSN276201200161U).

  • See Editorial on Page 1121

Abstract

An association of hepatitis C virus (HCV) infection with diabetes has been reported in many studies, but few have been population based and applied standard criteria for diabetes diagnosis. We examined this relationship using recent population-based data from the U.S. National Health and Nutrition Examination Survey. Adult participants (15,128) in the 1999-2010 surveys had data on diabetes status and serum HCV antibody (anti-HCV) or HCV RNA. Using American Diabetes Association criteria, diabetes was defined as a health care provider diagnosis, serum hemoglobin A1C (A1C) ≥6.5%, or fasting plasma glucose (FPG) ≥126 mg/dL, prediabetes as A1C 5.7%-<6.5% or FPG 100-<126 mg/dL, and normal glucose as A1C <5.7% and FPG <100 mg/dL. Odds ratios (ORs) for diabetes and prediabetes, comparing persons with HCV infection to those without, were adjusted for demographics, BMI, C-reactive protein, smoking, drinking, and blood transfusion before 1992. Among participants without diabetes, we compared mean insulin resistance (IR), estimated using homeostasis model assessment (HOMA-IR), by HCV status. The overall prevalence of anti-HCV+ was 1.7%, of HCV RNA+ 1.1%, of diabetes 10.5%, and of prediabetes 32.8%. The prevalence of diabetes and prediabetes did not differ by HCV status. In multivariate-adjusted analysis, diabetes remained unassociated with anti-HCV (OR, 1.0; 95% confidence interval [CI]: 0.6-1.7) or with HCV RNA (OR, 1.1; 95% CI: 0.6-1.9). In contrast, elevated alanine aminotransferase and gamma glutamyltransferase activities were associated with diabetes regardless of HCV status. HOMA-IR was not associated with HCV markers in unadjusted or multivariate-adjusted analyses (P > 0.05). Conclusion: In the U.S. population, HCV was not associated with diabetes or with IR among persons with normal glucose. Previously reported relationships of HCV with diabetes were possibly attributable to the effect of elevated liver enzymes. (Hepatology 2014;60:1139–1149)

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