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

The effect of clofibrate (1.5 g/day) on different plasma proteins and on components of the hemostatic system was studied in eight men with either mild diabetes mellitus or cardiosclerosis. Before treatment, the subjects were investigated weekly on five occasions. The means of these determinations were compared with the values observed after 2, 6 and 14 weeks of treatment. During the treatment albumin and transferrin increased significantly while orosomucoid, ceruloplasmin, beta1 E-globulin, IgA, IgM and fibrinogen decreased significantly. The decreases of the last proteins in per cent were found to be associated with each other in single subjects, i.e. a subject who reacted with a certain degree of change in one protein tended to react in a similar way with regard to the other proteins. A correlation was observed between the concentration before the treatment and the decrease in concentration during the treatment for ceruloplasmin, IgG, IgA, IgM and fibrinogen. The fibrinolytic activity increased significantly. Plasminogen decreased after 6 weeks and increased after 14 weeks of treatment. Platelet adhesiveness was not influenced.
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PMID:Effect of clofibrate on plasma proteins including components of the hemostatic mechanism. 13 Oct 8

A 59 year old woman with insulin-dependent diabetes mellitus and chronic diarrhea was found to have mild steatorrhea, selective plasma IgA deficiency and adrenal insufficiency. Significant adrenal secretion of corticosteroids resulted only after prolonged stimulation with large doses of exogenous ACTH. Plasma ACTH levels were not elevated during clinical adrenal insufficiency or after metyrapone administration but did respond normally to vasopressin and insulin-induced hypoglycemia. These studies were interpreted as showing both primary adrenal insufficiency and impaired pituitary reserve for ACTH secretion in response to the feedback stimulus. No deficiency was found in secretion of other pituitary tropic hormones. Jejunal biopsy showed a lack of IgA-containing plasma cells. With cortisone replacement, diarrhea subsided and a malabsorption pattern on a film of the small bowel was no longer seen. IgA deficiency has been noted frequently with steatorrhea but rarely with diabetes and only once previously with adrenal insufficiency.
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PMID:Atypical adrenal insufficiency with failure of the pituitary feedback receptor. A case with associated diabetes mellitus and selective IgA deficiency with steatorrhea. 17 48

Metabolic disorders and immunological factors are discussed in connection with the pathogenesis of diabetic microangiopathy. Renal biopsies were obtained from 22 diabetics (8 women aged 18 to 53, 14 men aged 15 to 52). 7 of the 22 patients had been suffering from diabetes for 2 weeks to 3 years, 10 for 7 to 25 years, 2 showed a pathological glucose-tolerance test, i.e., they had been "latent" diabetics, and 3 patients, had been so-called "potential" subjects of diabetes due to hereditary traits or delivery of big babies. They were examined by light miroscopy as well as by immunofluorescence microscopy. A number of cases were chosen for the differentiation and counting of glomerular cells (n=8) as well as for electron microscopic (n=7) and polarizing-microscopic (n=6) examinations. Histologically, focal proliferations of mesangial cells as well as an increase in mesangial substance in the glomeruli was found in all cases, although in a varying degree of intensity. These results were confirmed by both the glomuerular cell count and electron-microscopic examination. Immunofluorescence microscopy made it possible to detect frequently both IgA (9/17) and IgG (9/17), usually in either linear or mesangial arrangements whereas it was less frequently possible to detect IgM (1/17) and albumin (1/8) and impossible to detect beta1C in the glomerulus. Labeled insulin was detected five times in the glomerulus. Polarizing-microscopic measurements made in order to discover possible submicroscopic variations in the structure of GBM showed deviations in the average values of anisotropic indices from the controls in the group of long-term diabetics only. The pathogenesis of diabetic microangiopathy may be described as an inflow of immunoglobulins and serum proteins into the mesangium because of an alteration of the capillary endothelium, the mesangial cell being thus caused to overfunction, proliferate and produce an excess of mesangial matrix. In prolonged diabetes the mesangial cell, so far as its own metabolism is concerned, will finally be affected to the point where its power of synthesis is modified in the sense of an excess and/or faulty composition of GBM (glomerular basement membrane).
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PMID:Renal biopsies performed on diabetics. 33 62

Renal biopsies obtained from 22 patients with diabetes (8 women, mean age 38.5 years; 14 men, mean age 27.3 years)--including patients with potential, latent, short-term, and long-term diabetes--were examined by light microscopy as well as by immunofluorescence microscopy. Histologically, segmental and focal proliferation of mesangial cells as well as a mesangial broadening and an increase of substance deposited in the mesangium was found. These findings well documented by cell counting an differentiation are described in detail elsewhere (see Sorger et al. 1976 Immunhistochemically, we detected most frequently IgA (9/17) and IgG(9/17), usually in a linear or mesangial pattern, less frequently IgM (1/17). We failed to detect beta 1C and IgE in the glomerulus. Labeled insulin was demonstrated 5 times. Out of the plasmaproteins albumin, fibrinogen, transferrin, and beta-lipoproteid only albumin was perceptable. We consider the deposition of immunglogulins and serum-proteins in the glomerular filter to be an unspecific stimulation of proliferation of the mesangial cells being caused by overfunction and obviously produce an excess of the mesangial matrix.
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PMID:[Immunohistochemical findings in renal biopsies performed on diabetics (author's transl)]. 33 12

A 51-yr-old, nonobese, male patient presented with hyperglycemia and a recent 40-pound weight loss. Severe insulin resistance was documented in studies in which high amounts of insulin were infused using the Biostator GCIIS. Diabetic control was finally achieved with subcutaneous injections of 470 U of insulin per day. Positive laboratory findings included a mild pancytopenia, elevated erythrocyte sedimentation rate, decreased C3 and properdin, and increased IgA. Antinuclear or other autoantibodies were not present. Insulin antibody levels were within the range usually present in insulin-treated diabetic patients. Acanthosis nigricans was not present. Incubation of the patient's serum with IM-9 lymphoblastoid cells revealed that an insulin receptor antibody was present in a serum dilution of 1:80. Insulin-resistant diabetes mediated by insulin receptor antibodies may present in patients with immunologic findings but without overt dermatologic stigmata.
Diabetes Care
PMID:Insulin-resistant diabetes with insulin receptor autoantibodies in a male patient without acanghosis nigricans. 51 Jan 20

There is an increased prevalence (P less than 0.001) of IgA deficiency in children with juvenile-onset insulin-dependent diabetes mellitus (9/366) but not in adults with insulin-dependent diabetes (0/421). The juvenile diabetics with IgA deficiency have other immune-associated diseases, such as thyroiditis and chronic active hepatitis, and have a history of infections. Four of the nine IgA-deficient diabetics we studied have autoantibodies to endocrine organs. Seven of eight have the HLA-B8, a proportion significantly (P less than 0.05) greater than control populations. Based on the clinical findings of IgA deficiency and multiple autoantibodies in patients with ataxia-telangiectasia and chronic mucocutaneous candidiasis, diseases associated with thymus deficiency, we suspect that thymus deficiency and autoimmunity may play a role in the pathogenesis of some types of juvenile-onset diabetes mellitus. In addition, an excess morbidity of the IgA-deficient juvenile diabetic population may explain the lack of IgA deficiency in older insulin-dependent diabetic individuals.
Diabetes 1978 Nov
PMID:Immunopathology of juvenile-onset diabetes mellitus. I. IgA deficiency and juvenile diabetes. 72 Jul 69

Inflammatory disorders of the salivary glands cause marked abnormalities in secretion of immunoglobulins. The changes are reversible, however, in a relatively short period of time. More subtle changes in immunoglobulin transport are present in such diseases as Sjogren's syndrome and diabetes. No changes are discernable in alcoholic cirrhosis. Apparently salivary gland basement membranes are much more resistant to derangement than plasma membranes and the secretory IgA system can continue to operate in the face of numerous affronts. If nothing else these findings suggest that vaccination procedures in the region of the salivary glands may produce an inflammatory response, but it would be readily reversible. In addition, one could anticipate a functioning s-IgA system even in salivary glands with alterations in electrolyte transport. It is difficult to anticipate the situation in immunologically compromised patients, such as those on hemodialysis. Fortunately these patients represent a small population and for them at least, caries is a relatively minor concern.
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PMID:Salivary immunoglobulins in diseases affecting salivary glands. 74 16

Subpopulations of peripheral lymphocytes were studied in 26 children with insulin-treated juvenile diabetes and in 27 control children of comparable age. T-lymphocytes were quantitated by spontaneous rosette-formation with sheep erythrocytes and B-lymphocytes by indirect immunofluorescence with the use of monovalent, fluorescein-labeled rabbit antiserum specific to the heavy chains of human IgG IgM, or IgA. No significant quantitative difference in subpopulations of the peripheral lymphocytes, T-cells, and B-cells with IgG, IgA, or IgM markers found between children with juvenile diabetes and the control group, although the B-lymphocytes with IgG or IgA markers tended to be higher and those with IgM markers lower in the diabetic than in the control group.
Diabetes 1976 Feb
PMID:Subpopulations of peripheral lymphocytes in juvenile diabetes. 76 77

A study of serum euglobulins carried out in 26 patients with diabetes mellitus and in 14 healthy persons permitted to detect definite differences between sick and healthy individuals. In the patients with diabetes mellitus (most distinctly in those with microangiopathies) the level of soluble and insoluble in the phosphate buffer euglobulins was greater than in the healthy persons. The microprecipitation reaction and immunoelectrophoresis with the monospecific immunoglobulins (IgA, IgM and IgG) more frequent and higher titers demonstrated IgA and IgG in diabetic patients. More pronounced heterogeneity (particularly distinct in the subfraction of euglobulins insoluble in the phosphate buffer) than in healthy individuals was revealed in the patients with diabetic microangiopathies by disc electrophoresis in polyacrylamide gel. The data obtained served as the basis for the search in the serum euglobulins of the patients with diabetes of compounds possibly possessing the antigenic properties, capable of producing antibodies and immune complexes, i.e. the immunological factors taking part in the vascular wall injury.
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PMID:[Blood serum euglobulins in diabetes mellitus and diabetic microangiopathies]. 84 71

Six families were studied which included 11 members with dermatitis herpetiformis (DH) and three with coeliac disease (CD). Proximal jejunal biopsies performed on 20 relatives revealed villous atrophy in eight. Of these eight, two, both siblings of patients with DH, had a history of juvenile CD. Determinations of histocampatibility (HLA) antigens showed that HLS-B8 occurred in all six families although two patients with DH and one relative with a history of juvenile CD lacked this antigen. In one family the haplotype A1,B8 was associated with DH, villous atrophy, juvenile diabetes and Addison's disease. Skin biopsy failed to reveal IgA in any of the 44 relatives studied for this immunoglobulin. Antireticulin antibody was detected in the sera of seven (17%) relatives.
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PMID:Family studies in dermatitis herpetiformis. 99 11


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