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Evaluation of a Diagnostic Algorithm for Hereditary Hemochromatosis in 3,500 Patients With Diabetes

¹ Klinikum Suedstadt Rostock, Center for Vascular Medicine, Rostock, Germany
² Clinic for Diabetes and Metabolic Diseases Karlsburg, Karlsburg, Germany
³ Institute of Clinical Chemistry and Laboratory Medicine, University of Rostock, Rostock, Germany
⁴ Clinic for Transplantation Hepatology, University of Muenster, Muenster, Germany

Address correspondence to Dr. Jan-Uwe Hahn, Clinic for Diabetes and Metabolic Diseases Karlsburg, Greifswalder Str. 11, 17495 Karlsburg, Germany. E-mail: januwe.hahn@t-online.de

The first 20% of the full text of this article appears below.

Hereditary hemochromatosis may lead to hepatic cirrhosis, cardiomyopathy, diabetes, arthritis, and impotence (1, 2). In the Caucasian population, HFE gene mutations (C282Y and H63D) are present in the majority of patients demonstrating phenotypic expression (3–6). Conversely, the clinical penetrance in mutation carriers is low (7).

In the precirrhotic stage, 20% of hemochromatosic patients demonstrate hyperglycemia, with the prevalence increasing to >70% in the presence of liver cirrhosis (8). Two mechanisms contribute to the development of hyperglycemia and diabetes. Liver iron overload leads to insulin resistance, and the pancreatic ß-cell iron accumulation results in cell damage and diminished insulin secretion (1). The prevalence of genotypic and phenotypic hemochromatosis is higher in diabetic versus nondiabetic populations (9–11).

In an attempt to distinguish patients with hemochromatosis-associated secondary diabetes from other forms of diabetes, we applied a screening program to diabetic patients aged 40 . . . [Full Text of this Article]

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				A. R. Gosmanov and G. E. Umpierrez A Patient with Diabetes, Hepatitis C Virus Infection, and Hemochromatosis Gene Mutation Clin. Diabetes, October 1, 2008; 26(4): 174 - 176. [Full Text] [PDF]