Diabetes Mellitus and Idiopathic Hemochromatosis

Sp, Balcerzak; Dh, Mintz; Mp, Westerman

doi:10.1097/00000441-196801000-00010

Cited by 33 publications

(7 citation statements)

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“…Thus the hypothesis that common diabetes could share some genetic background with IH diabetes was proposed. This is in agreement with published data (Boulin & Bamberger 1953, Balcerzak et al 1968, Pozza & Ghidoni 1968, Dymock et al 1972) but denied by Simon et al (1976a).…”

supporting

confidence: 94%

HLA‐A3, B7 linkage disequilibrium in hemochromatotic patients with or without insulin dependent diabetes

et al. 1981

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Sixty-six idiopathic hemochromatotic French patients were HLA-A, B typed. The previously known strong association with A3 was confirmed (RR = 10.6, P and our results indicate clearly that a gene implicated in idiopathic hemochromatosis (IH) determinism is located in the HLA-A region.The linkage disequilibrium between A3 and B7 was found to be far greater in IH patients than in controls. The authors have therefore hypothesized that this might be due to a selective advantage of this haplotype in IH. The A3, B7, Dw2 HLA haplotype has been shown to exert a protective effect against common insulin dependent diabetes (IDD). Thus the patients were divided into two groups according to the presence or absence of a definite IDD. B7 was found more frequently in IH patients without IDD but the difference is not significant.In this context, the strong linkage disequilibrium between A3 and 8 7 might be due to the protective effect of the B region of this haplotype against IH secondary IDD.

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supporting

confidence: 94%

HLA‐A3, B7 linkage disequilibrium in hemochromatotic patients with or without insulin dependent diabetes

et al. 1981

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“…It is still unclear whether the diabetic disease is inherited or at least related to familial factors, or if the iron overload has a direct diabetogenic role. Epidemiological studies have led to opposite conclusions [3][4][5][6][7]. However, large prospective studies by Simon at al.…”

mentioning

confidence: 99%

The haemochromatotic human pancreas: a quantitative immunohistochemical and ultrastructural study

et al. 1987

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Insulin, glucagon, somatostatin and pancreatic polypeptide cells were quantified after immunoperoxidase staining in sections of pancreases obtained from nine control subjects and seven diabetic patients with primary or secondary iron overload. One was normoglycaemic, two had glucose intolerance and four presented insulin-requiring diabetes. The whole pancreas was studied, taking into account the heterogeneous distribution of the endocrine cells. In the diabetic patients, the weight of the pancreas tended to be lower. Iron overload predominated in the exocrine tissue, whereas in islets iron concentration was quite variable from case to case. At the Haemalun-Eosine staining the histological appearance of the islets was normal, their shape and size being unchanged; amyloid deposits were absent, as were atrophic islets. Immunoperoxidase staining revealed a severe reduction in the number of immunoreactive B cells in the four diabetic patients. The mass of immunoreactive B cells was calculated from their volume density and from the weight of each lobe of the pancreas. It averaged 950 mg in control subjects, 1580 mg in the normoglycaemic patient, 1010 mg in patients with glucose intolerance and 180 mg in insulin-requiring diabetic patients. The electron microscopic examination, performed in four cases, revealed that the iron deposits were restricted to B cells and associated with progressive loss of their endocrine granules. The study shows that the pancreatic islet abnormalities in iron overloaded diabetic patients are completely different from those of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetic patients. This constitutes a further argument for a specific role of iron in the pathogeny of diabetes in haemochromatotic patients.

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“…is due to the pancreatic lesions resulting from the pancreatic iron overload; therefore diabetes is usually considered as secondary to pancreatic pathology [1][2][3][4]. However some recent data suggest that pancreas iron overload is not the main cause of glucose intolerance, that diabetes may be regarded as related to the inherited type and that iron overload may only favour its onset [5][6][7].…”

mentioning

confidence: 99%

Glucagon secretion in diabetic patients with idiopathic haemochromatosis

et al. 1977

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The aim of the present investigation was to determine in patients with idiopathic haemochromatosis whether diabetes is of the primary type or secondary to pancreatic injury due to iron deposition. For this purpose, plasma glucagon concentrations were determined following arginine infusion or an oral glucose load in eight patients with diabetes and idiopathic haemochromatosis. The enhanced glucagon response to arginine and the nonsuppressibility of glucagon secretion by oral glucose found in these patients were similar to the results found in the same tests performed in our previous series of patients with "idiopathic" diabetes and at variance with those reported by others in patients with chronic pancreatitis.

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Diabetes Mellitus and Idiopathic Hemochromatosis

Cited by 33 publications

References 0 publications

HLA‐A3, B7 linkage disequilibrium in hemochromatotic patients with or without insulin dependent diabetes

HLA‐A3, B7 linkage disequilibrium in hemochromatotic patients with or without insulin dependent diabetes

The haemochromatotic human pancreas: a quantitative immunohistochemical and ultrastructural study

Glucagon secretion in diabetic patients with idiopathic haemochromatosis

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