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Association between Hepatitis C Virus Infection and Diabetes Mellitus

    1. [1] Johns Hopkins University

      Johns Hopkins University

      Estados Unidos

  • Localización: Epidemiologic reviews, ISSN 0193-936X, ISSN-e 1478-6729, Vol 23, 2, 2001, págs. 302-312
  • Idioma: inglés
  • Enlaces
  • Resumen
    • A number of infectious agents have been linked to chronic diseases, including the linkages of human immunodeficiency virus with acquired immunodeficiency syndrome, Epstein-Barr virus with Burkitt's lymphoma, human papillomavirus with cervical cancer, and hepatitis B virus (HBV) with hepatocellular carcinoma (1-4). Both biologic plausibility and strong epidemiologic evidence were used to demonstrate that these infectious agents caused the associated chronic disease. Epidemiologic associations can be made by detecting either an increased prevalence of the chronic disease among persons with the infection or an increased prevalence of the infection among persons with the chronic disease. The biologic link is strengthened by demonstration of the infectious agent in the diseased tissues, but it can also be made indirectly by observation of overlapping features in the pathophysiology of the infection and the chronic disease.

      Hepatitis C virus (HCV) infection is mainly a disease of the liver. However, HCV has also been linked to a variety of chronic conditions involving several other organ and tissue systems, including the kidneys and skin. For some of these diseases, there is strong epidemiologic evidence and biologic plausibility, while for others there is only epidemiologic evidence. Diabetes mellitus is one such chronic condition that has recently been associated with HCV infection.

      In the past 5 years, at least 22 reports either supporting (n = 19) (19, 28-37, 40, 41, 45^7 , 52-54) or refuting (n = 3) (38, 49, 50) an association between these two conditions have been published. However, the literature on this subject and the potential biologic mechanisms involved have not been recently reviewed. This review considers the existing literature with respect to both the epidemiologic evidence and the biologic evidence for a causal relation between these two common conditions


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