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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The possible relationship between Lewis red cell groups and secretor status and diabetes mellitus has been investigated in diabetic patients from Northwestern Ethiopia. The Lewis negative phenotype [Le(a-b-)] showed similar frequencies in diabetics and a control sample. Determination of the secretor status revealed a tendency to higher non-secretor rates in diabetics, particularly of the insulin-dependent type, in comparison with non-diabetic Ethiopians. A lack of effective immune protection from secretory IgA antibodies as a plausible explanation for the relationship between non-secretor status and IDDM is discussed. However, the available data from our study showed no statistically significant association between secretor state and IDDM. Without a detailed genetic characterization of our diabetic patients (HLA association data) it will be difficult to define precisely the postulated contribution of the Se gene to the aetiopathogenesis of IDDM.
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PMID:ABH-secretion and Lewis red cell groups in diabetic and normal subjects from Ethiopia. 381 5

Direct immunofluorescence examination was performed on peripheral nerve from 16 patients with diabetes mellitus and 53 additional patients with peripheral neuropathy of diverse cause. Six nerves from patients with diabetes mellitus yielded positive findings: 4 had granular and lamellar deposition of IgM within the perineurium (of which 2 also had fibrinogen, IgA, C3, and albumin and 1 also had IgG); 1 had IgM, C3, and C4, and perineurial fibrinogen; the sixth contained linear perineurial C3 and fibrinogen. These 6 nerves contained axonal degeneration (3), axonal degeneration with chronic demyelination (1), microvasculitis with wallerian degeneration (1), and no pathological change (1). Sixteen of 53 nerves from nondiabetics yielded positive findings with immunofluorescence, possibly as a result of vascular leakage or as a manifestation of impaired removal of plasma proteins. The deposition of immunoreactants, as well as other plasma proteins, in peripheral nerve from patients with diabetes mellitus probably represents a "trapping" phenomenon reflecting altered basement membrane permeability. Alternatively, the changes could reflect a defect in the blood-nerve barrier in diabetic microangiopathy.
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PMID:Direct immunofluorescence findings in peripheral nerve from patients with diabetic neuropathy. 389 Jul 1

Plasma Antithrombin III (AT III) has been shown to be elevated in certain conditions like diabetes mellitus and coronary artery disease as well as in situations where there is increased platelet turnover. This study attempts to define the role of platelet injury in Clinical Nephrology and assesses the clinical value of ATT III. In IgA Nephritis, plasma AT III levels (105 +/- 10%) in 97 patients were higher than those of normal controls (96 +/- 5%) (p less than 0.0005). AT III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.01), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised AT III had more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA on IMG (p less than 0.02) when compared to patients with normal AT III levels. The data suggest that plasma AT III may serve as a marker of disease activity in IgA nephritis. Plasma AT III levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). Pre and post hemodialysis platelet counts however did not change significantly. In peritoneal dialysis patients, AT III levels which were normal before dialysis, increased significantly after peritoneal dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.
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PMID:Galloway memorial lecture. Platelet injury and antithrombin III in clinical nephrology. 389 86

Post-mortem samples of parotid gland were obtained from 15 patients with a history of diabetes mellitus for a minimum of 5 years, and from 15 age- and sex-matched controls. The tissue was studied by direct immunofluorescence for abnormal binding of selected serum proteins, including IgG, IgM, IgA, C3, fibrinogen, polyvalent immunoglobulin and albumin, to acinar and ductal basement membranes of the gland. Thickness of these basement membranes was also assessed using a calibrated magnifier on uniformly enlarged photomicrographs of the tissue which had been stained by the chromotrope silver methenamine method to highlight basement membranes. Results of this investigation revealed parotid gland basement membrane abnormalities in all diabetic subjects as indicated by the binding of IgG, albumin and polyvalent immunoglobulins to ductal and acinar basement membranes. These basement membranes were uniformly negative in control subjects for the binding of all serum proteins tested. Binding of IgA was also noted in 7 of 15 experimental subjects, with 6 of these representing Type I diabetics. Basement membrane measurements revealed no difference in thickness between diabetic and non-diabetic subjects. Variations in parotid diabetic basement membranes evidenced in this study further substantiate the idea that membranopathy in this disease is systemic in nature.
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PMID:Parotid gland basement membrane variation in diabetes mellitus. 392 79

The frequency of various autoimmune features in 14 patients with insulin-resistant diabetes mellitus (type B) was reviewed. Twelve patients had leukopenia, high titers of antinuclear antibodies (speckled pattern), and hypoalbuminemia; 11 had elevated serum levels of IgG and high erythrocyte sedimentation rates; 7 had proteinuria and high serum levels of antibodies to DNA; and 5 had alopecia and elevated serum levels of IgA. Lupus erythematosus preparations were negative in all patients. Eight patients met the conventional criteria for the diagnosis of systemic lupus erythematosus. Three patients developed renal involvement while under care at the National Institutes of Health. Kidney tissue samples showed proliferative and membranous glomerulonephritis, tubulointerstitial nephritis, and electron-dense deposits similar to those of lupus nephritis. The lupus nephritis in these 3 patients appeared to be independent of the level of insulin-receptor antibody and glucose dysmetabolism. This study documents the presence of systemic lupus erythematosus in a large proportion of patients with insulin resistance due to autoantibodies to insulin receptors and emphasizes that careful monitoring of such patients for major complications of lupus nephritis is warranted.
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PMID:Lupus nephritis and other autoimmune features in patients with diabetes mellitus due to autoantibody to insulin receptors. 396 55

In a prospective study of 70 unselected patients with chronic liver disease, clinical signs of a peripheral neuropathy were observed in 13 patients. Abnormal nerve conduction was demonstrated in nine of these and in one further patient who had no abnormal neurological signs. The occurrence of a neuropathy (in patients with cryptogenic cirrhosis, haemochromatosis, active chronic hepatitis as well as in alcoholic cirrhosis) could not be related to liver function, although it was associated with higher IgA and IgM values. Clinical diabetes was present in six of the 14 patients with neuropathy but there was no relation in the non-diabetic patients between neuropathy and minor impairment of carbohydrate tolerance. Those with neuropathy had a significantly higher incidence of oesophageal varices and there was also a relationship to a history of previous encephalopathy. Sural nerve biopsy was carried out on 14 patients, eight of whom had clinical or electrodiagnostic evidence of neuropathy. Single nerve fibres were examined by teasing and in all nerves histological evidence was found of an indolent process which had damaged whole Schwann cells and which resulted in demyelination and remyelination. Diabetic angiopathy was not seen and axonal degeneration, which was never severe, was found in all disease groups equally.
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PMID:Peripheral neuropathy in chronic liver disease: clinical, electrodiagnostic, and nerve biopsy findings. 433 71

A complex between serum albumin and immunoglobulins was observed on immunoelectrophoresis in six patients. Two patients with multiple myeloma had monoclonal IgA-albumin complexes; one of these complexes was formed by covalent bonds and the other by non-covalent bonds. Four patients displayed non-covalent IgG-albumin complexes: of these, one had multiple myeloma, two had been treated with nitrofurantoin for prolonged periods, and one had diabetes mellitus. The IgG-albumin complex of the last patient was subjected to a detailed immunochemical analysis. The albumin-specific antibodies were isolated by affinity chromatography and analysed, using a sensitive tritium labelling technique. The antibodies were polyclonal, complexed with serum albumin through their Fab portion, and showed a high specificity for the human albumin as compared with bovine and rabbit albumins. The serum albumin of two patients displayed an abnormal behaviour in reduced SDS-polyacrylamide gel electrophoresis (PAGE). The abnormal albumins had an apparent molecular weight of 52,000 and could react with rabbit anti-human serum albumin like the normal protein. No abnormal albumin could be detected in 20 other patients' sera, including nitrofurantoin-treated patients and normal controls. These findings suggest a possible role for an altered self-component in the triggering of a specific autoimmune reaction.
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PMID:Albumin-immunoglobulin complexes in human serum: classification and immunochemical analysis. 617 76

The clinical and laboratory research into the immunological status of children with diabetes mellitus in the stage of clinicometabolic decompensation and investigation of the function of the insular apparatus of the pancreas according to the IRI and C-peptide data were carried out in 115 children aged 3 to 14 years with diabetes mellitus and 30 normal children. The data obtained indicate dysfunction of the immunogenesis system in children with diabetes mellitus and reduction of the functional potentialities of the insular apparatus of the pancreas. The immunological status of children with diabetes mellitus was characterized by dysimmunoglobulinemia at the expense of elevation of the IgA and reduction of IgG levels, deficiency of T cells and decrease in their function, elevation of the B lymphocyte level, reduction in non-specific defence factors. The degree of the abnormalities cited was in agreement with the standing and degree of pathological process, the levels of IRI and C-peptide, and insulin therapy. The immunological tests are helpful in the detection of insulin resistance of the immune type and in administering appropriate therapy. Insulin administered exogenously stimulates the B-lymphocyte component of the immunopoiesis.
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PMID:[Characteristics of the immune system in children with diabetes mellitus]. 633 93

The relative contribution of monomeric and polymeric IgA was investigated in diabetic sera showing that 80-87% of IgA in diabetes are polymeric. A defective mechanism of hepatobiliary transport of IgA is suggested in diabetes mellitus.
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PMID:Serum hyper IgA in diabetes mellitus: I. Increase in the proportion of the polymeric to the monomeric form. 646 59

The relative contribution of secretory IgA, monomeric and polymeric IgA and IgA/secretory component-containing immune complexes was investigated in sera of diabetic patients. Secretory IgA and immune complexes containing IgA and secretory component seem to participate in the hyper-IgA of patients with Type 2 (non-insulin-dependent) diabetes only, suggesting an altered hepatic clearance via secretory component receptors on hepatocytes. In Type 1 (insulin-dependent) diabetes, the high serum IgA levels might be explained by an increase in IgA production in response to antigenic stimuli. Evidence is also accumulated that immune complexes containing IgA of mucosal origin may be involved in microangiopathy production in Type 2 diabetes.
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PMID:Contribution of secretory IgA, polymeric IgA and IgA/secretory component-containing circulating immune complexes to the serum hyper-IgA in diabetes mellitus. 647 89


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