title: [Importance of hereditary haemochromatosis in the care of diabetes mellitus].
abstract: Interactions of iron and carbohydrate metabolism were examined using results of the literature. Special attention was paid to the description of processes involving free radical production because both hereditary haemochromatosis and diabetes mellitus lead to complications by inducing oxidative stress. High levels of blood and tissue glucose produce an excess of electrons. This overload of tissues by electrons may reduce redox-active, non-haeme ferric iron to ferrous one evolving oxidative stress. Hereditary haemochromatosis may cause an elevation in the concentration of the intracellular redox-active iron in both the general and in the diabetic populations. The ratio of carriers (hetero- + homozygotes) of mutations for hereditary haemochromatosis may be as high as 30.4% in the general and 35.8% in the diabetic Hungarian populations. Some data support the possibility that these common forms of hereditary haemochromatosis mutation (HFE-C282Y and HFE-H63D)--even in the heterozygote form--elevate the tissue level of iron without manifesting the phenotype of classical hereditary haemochromatosis. Elevated tissue iron--in patients with already damaged organs due to other diseases e.g. diabetes mellitus--may cause a progression of the complications. On the other hand, hereditary haemochromatosis may lead to endothelial damage and this way hypertension may precede the manifestation of diabetes mellitus. On the basis of these, it may be supposed that elevation of blood pressure should be taken into consideration as one of the earliest clinical symptoms of hereditary haemochromatosis. A therapy-resistant state caused by the hereditary haemochromatosis may be found in diabetes mellitus and hypertension.
authors.affiliation: Altalános Orvostudományi Kar, II. Belgyógyászati Klinika és Nephrologiai Centrum. istvan.wittman@aok.pte.hu
authors.forename: István
authors.initials: I
authors.lastname: Wittmann
authors.forename: László
authors.initials: L
authors.lastname: Wagner
authors.forename: Lajos
authors.initials: L
authors.lastname: Markó
authors.forename: Mónika
authors.initials: M
authors.lastname: Tamaskó
authors.forename: Boglárka
authors.initials: B
authors.lastname: Laczy
authors.forename: Mohás
authors.initials: M
authors.lastname: Márton
authors.forename: Judit
authors.initials: J
authors.lastname: Cseh
authors.forename: Béla
authors.initials: B
authors.lastname: Melegh
mesh_terms: D001786:Blood Glucose / Q000378:metabolism; D048909:Diabetes Complications / Q000097:blood / Q000378:metabolism*; D018450:Disease Progression; D005609:Free Radicals / Q000378:metabolism; D005787:Gene Frequency; D005947:Glucose / Q000378:metabolism*; D006432:Hemochromatosis / Q000175:diagnosis / Q000453:epidemiology / Q000235:genetics / Q000378:metabolism* / Q000628:therapy; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I / Q000235:genetics*; D006801:Humans; D006814:Hungary / Q000453:epidemiology; D006973:Hypertension / Q000378:metabolism; D007501:Iron / Q000378:metabolism*; D008565:Membrane Proteins / Q000235:genetics*; D009154:Mutation; D018384:Oxidative Stress
chemical_list: D001786:Blood Glucose; D005609:Free Radicals; C103673:HFE protein, human; D000071020:Hemochromatosis Protein; D015395:Histocompatibility Antigens Class I; D008565:Membrane Proteins; D007501:Iron; D005947:Glucose