UMLS:C0011849 - FACTA Search

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

160 children and young adults (aged 7-21 years) and 84 diabetics (aged 2-19 years) were screened for thyroglobulin (TgA), thyroid microsomal (MsA), smooth muscle (SMA), parietal cell (PCA), reticulin (RA), glomerular (GIA) and mitochondrial (MA) antibodies. The diabetics were also screened for islet cell antibodies (ICA). The overall incidence of other antibodies than ICA at the lowest serum titre studied was 18.1 percent for healthy children and 30.9% for diabetic children. The elevation in diabetics is significant (p less than 0.01). Females were overrepresented in both groups and had the highest titres of antibodies. The age group 10-14 years was observed to be a special time at which antibody titres became positive. As compared with the controls, diabetics exhibited an increased incidence of MsA (4.4 and 11.9% respectively, p less than 0.001), PCA (5.0 and 10.7% respectively, p less than 0.05) and RA (3.8 and 9.5% respectively, p less than 0.05). The presence of ICA or the duration of diabetes showed no correlation with other autoantibodies. The results indicate that autoantibodies at a low titre are a common phenomenon. Diabetics seem to be susceptible to react against their own tissue, which is probably associated with their increased frequency of autoimmune diseases.
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PMID:Organ-specific antibodies in healthy and diabetic children and young adults. 675 72

Sera from 438 children were examined for autoantibodies to thyroid microsomes, thyroglobulin, pancreatic islet cells, gastric parietal cells, and adrenocortical cells by indirect hemagglutination and immunofluorescence techniques. A modification of the indirect hemagglutination technique allowed specific detection of low titers of antithyroidal antibodies. The subjects included a control group (117) with no known autoimmune disease, and children with disorders of the thyroid (88), insulin-dependent diabetes mellitus (201), Turner's Syndrome (24), and Addison disease (8). A subject's age at the time of disease onset and the race and sex were correlated with the prevalence of autoantibodies. The coincidence of autoantibodies to components of the thyroid with autoantibodies to gastric parietal cells was increased in children with disorders of the thyroid (94%, 18/19) over that observed in diabetes (29%, 4/14), Turner syndrome (0%), or Addison disease (0%), perhaps indicating different genetic propensities for the development of parietal cell antibodies in these groups. Islet cell antibodies were not found in subjects with Turner syndrome, nor were they more prevalent in white or black subjects with diabetes. The incidence of organ-specific autoantibodies in individuals without overt clinical disease may reflect an altered immunologic state that will lead eventually to autoimmune disease. Islet cell antibodies decline in prevalence in diabetes, whereas thyroid antibodies in disorders of the thyroid do not; this may reflect differences in the pathogenesis of these common autoimmune endocrine disorders in children.
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PMID:Organ-specific autoantibodies in children with common endocrine diseases. 703 35

The levels of triiodothyronine (T3), thyroxine (T4), TTH, STH, free triiodothyronine index T3F/T3/T4, as well as the titers of antibodies to microsome-membranous antigen and thyroglobulin, were studied in thyrotoxic patients with hereditary predisposition to endocrine diseases (thyrotoxicosis, goiter, diabetes mellitus) and in subjects without such heredity. Peculiarities of the disease development and endocrinopathy distribution among their relatives were investigated. More pronounced disorders in thyroid hormone metabolism and humoral immunity state were seen in thyrotoxic patients with hereditary predisposition to endocrine diseases. In comparison with those of the subjects without this heredity. The risk of diabetes mellitus development was detected in thyrotoxic patients predisposed to diabetes mellitus. Clinical manifestations of thyrotoxicosis (the disease severity, goiter of the IVth sage, exophthalmos) were also more evident in subjects predisposed to endocrine diseases.
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PMID:[Characteristics of the clinical aspects, and hormonal and immunological status of thyrotoxicosis patients with a hereditary predisposition to endocrine diseases]. 712 51

Circulating antibody titers (1:20 to 1:2560) against thyroglobulin were demonstrated in 48% of pet dogs with hypothyroidism by the chromic chloride passive hemagglutination test. Four of six dogs with acanthosis nigricans (1:20) and one of six male dogs with hyperestrogenism (1:40) had low titers of antibody against thyroglobulin whereas clinically normal pet dogs and dogs with other selected endocrinopathies (hypoadrenocorticism, cortisol-excess, diabetes mellitus) or obesity were consistently negative. Circulating immune complexes evaluated by the mastocytoma cell-assay were present in the sera of 20% of pet dogs with hypothyroidism but were absent in clinically normal dogs. Although variations in dose significantly altered the quantitative response of the thyroid gland to thyrotropin the qualitative pattern of response was similar for T3 but not T4 in clinically normal laboratory beagles. The peak increases for serum triiodothyronine and thyroxine were observed either at eight (0.1 and 0.2 I.U bTSH/5 lbs) or 12 (1.0 I.U. bTYSH/5 lbs) hours postthyrotropin. Dogs with naturally occurring hypothyroidism had a decreased serum T3 and T4 at baseline and eight hours postthyrotropin (1.0 I.U. bTSH/5 lbs) compared to clinically normal pet dogs, laboratory beagles and dogs with other clinical endocrinopathies. The consistent lack of a significant increase of serum T3 and T4 in response to thyrotropin was necessary for the separation of certain hypothyroid from euthyroid pet dogs in which the baseline level of thyroid hormones were equivocal.
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PMID:Biochemical and immunological investigations on hypothyroidism in dogs. 740 88

Necrobiosis lipoidica (NL), a skin disease, is associated with insulin-dependent diabetes mellitus (IDDM). Natural autoantibody (NAb) activity in sera from 16 patients suffering from NL, with or without IDDM, was compared to that in sera from 41 patients with IDDM and 43 healthy controls. Isotype-specific enzyme-linked immunosorbent assays (ELISAs) were used to detect NAbs against actin, myosin, keratin, desmin, troponin, tropomyosin, thyroglobulin, insulin, single-stranded DNA and the hapten trinitrophenyl. NAb activity was significantly higher in sera from patients with NL (either with or without IDDM), compared with that detected in sera from patients with IDDM which was similar to that of healthy individuals. High proportion of NL sera exhibited increased IgG anti-tropomyosin (69%), anti-troponin, anti-desmin and anti-keratin (50% each), anti-insulin (44%) and anti-trinitrophenyl (31%) activities, as well as increased IgA and IgM anti-keratin activities (26% and 31%, respectively). The great majority (88%) of positive sera were polyreactive and contained NAbs, polyspecific and monospecific (as demonstrated by immunoadsorption studies), belonging to more than one isotype; there was no predominant serological reactivity pattern. In conclusion, increased NAb activity to cytoskeleton proteins is associated with the dermatological disease NL and not to the overlapping autoimmune disease (IDDM). The origin and significance of these NAbs is discussed.
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PMID:Increased natural autoantibody activity to cytoskeleton proteins in sera from patients with necrobiosis lipoidica, with or without insulin-dependent diabetes mellitus. 757 89

To clarify the value of autoantibodies as risk factors of complications in various endocrine abnormalities, the incidence of autoantibodies to thyroid microsomal antigen (ATMA), thyroglobulin, and the surface antigens of the rat islet, adrenal cortex, adenohypophyseal cells and human skin fibroblasts was studied in patients with insulin-dependent mellitus (IDDM), at the onset of the disease and during one-year insulin therapy, non-insulin-dependent diabetes mellitus (NIDDM), Hashimoto thyroiditis, Graves' disease, diabetes associated with thyroidal dysfunction, euthyroid polynodular goiter, Schmidt and polyglandular syndromes and in the population. The antibodies were determined by ELISA. Polyclonal activation of the immune system was found in all abnormalities, except in polyglandular in children. The proportion of patients with more than one type of antibodies was minimal (26.4%) in IDDM and maximal (62.0%) in Graves' disease. Among IDDM patients, polyclonal activation of the immune system was observed more often in women than in men (48.5 vs 8.5%). The persistence of antibodies to fibroblasts in IDDM patients was associated with the development of vascular complications. The latter were observed in 4 of 7 patients who had these antibodies during a year and in none of negative patients. Thus, fibroblast antibodies may have a predicative significance for the development of late diabetic complications. The highest prevalence of these antibodies was discovered in Graves' disease (37.9%) wherein the antibodies may be involved in the development of exophthalmus and pretibial mixedema. Thyroidal dysfunction developed in all IDDM patients with ATMA preserved during a year and in none ATMA-negative patients.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Humoral autoimmunity markers in autoimmune endocrine diseases]. 774 56

Uncoated spherical hydrogel microspheres (calcium alginate, nominal M(r) exclusion of > 600 kD) 800-900 microns in diameter were employed to prevent immune rejection of discordant islet xenografts isolated from pigs and cows. The islets were immobilized in the microspheres and injected into the peritoneum of 14 nonimmunosuppressed streptozotocin (STZ)-induced diabetic C57BL/6J mice. Four recipients received islet grafts from bovine calves, and 10 received islet grafts from pigs. In the control group of 15 diabetic mice implanted with nonencapsulated islets, 6 received i.p. porcine islets and 5 received i.p. bovine islets, whereas remaining 4 received porcine islets under the kidney capsule. Plasma glucose concentrations in recipients of the alginate-encapsulated islets promptly dropped from a preimplantation value of 498 +/- 47 (mean +/- SEM) to 142 +/- 6 (bovine) and 178 +/- 7 mg/dl (porcine) during the first wk. All the animals sustained these levels for at least 1 mo. Two mice implanted with bovine islets subsequently reverted to diabetes (plasma glucose > 250 mg/dl) at 43 days postimplantation. The remaining grafts maintained function for > 10 wk. In contrast, nonencapsulated islets failed to function, or sustained euglycemia for < 4 days. Mice receiving encapsulated islets showed a 23-38% gain in body weight during the first mo after implantation, compared with < 1% (P < 0.002) and 32% (P = 0.84) for the untreated diabetic (n = 6) and normal control (n = 6) groups. Immunohistochemical staining of long-term grafts (> 10 wk) revealed viable islets, with well-granulated alpha, beta, and delta cells; the external surfaces of the microreactors were free of fibrotic overgrowth and exhibited only occasional host cell adherence. Uptake studies with IgG and thyroglobulin (M(r) of 669 kD) suggest that the microreactors were permeable to molecules with a molecular weight of up to > 600 kD (including the various proteins of the complement system, M(r) of 24-570 kD). Spheres implanted in the peritoneum after only 1 wk stained positive for both IgG and for the C3 component of complement. These findings suggest that prolonged survival of discordant xenografts of porcine and bovine islets in the STZ diabetic mouse model can be achieved with uncoated alginate microspheres that are permeable to IgG and complement. The question of whether similar results can be achieved with uncoated alginate microspheres in higher animals remains to be fully determined.
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PMID:Xenotransplantation of porcine and bovine islets without immunosuppression using uncoated alginate microspheres. 777 Sep 22

We have postulated over many years that autoimmune thyroid diseases (AITD) are disorders of immunoregulation due to antigen specific defect(s) in suppressor (regulatory) T (Ts) lymphocyte function. Despite earlier skepticism, there is recent increased evidence to support this view. Several investigators working with animal models have demonstrated T lymphocyte subsets that are regulatory, i.e., will prevent AITD; conversely, depletion of these cells precipitates the lesion in the experimental models. These cells have been shown to be inadequately activated by specific antigen. In human AITD, recent studies have demonstrated that CD8+ (suppressor/cytotoxic) and CD8+CD11b+ ("pure suppressor") cells are activated by irrelevant antigen normally, but are significantly less well activated in response to thyroglobulin or thyroperoxidase. In further similar studies, CD8+ cells from patients with Graves' disease (GD) are induced normally in response to glutamic acid decarboxylase-65 (GAD-65), the putative beta cell antigen important in insulin-dependent diabetes mellitus (IDDM), but significantly less to synthetic TSH receptor (TSHR). Conversely, CD8+ cells from patients with IDDM are activated normally in response to TSHR, but significantly less to GAD-65. While these reductions in activation are partial only, and other additive factors playing on the immune system may be necessary to precipitate AITD, this disorder in the activation of Ts cells may be fundamental to the development of these disorders. This in turn may be due to molecular disturbances in MHC-related genes that dictate the mechanisms of presentation of specific antigen.
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PMID:Immunoregulation in autoimmune thyroid disease. 783 79

To elucidate the role played by interferon-alpha (IFN alpha) in the pathogenesis of autoimmune endocrine disease, we determined the autoantibody status, thyroid function test results, hemoglobin-A1c levels, and clinical symptoms of 58 patients who received IFN alpha for treatment of chronic active type C hepatitis. Each patient was treated for 6 months with a total dose of 391 +/- 140 x 10(6) U (mean +/- SD). Thyroid microsomal and/or thyroglobulin antibodies newly appeared or were increased in titer in 6 patients, 2 of whom developed hypothyroidism during IFN alpha therapy. Neither islet cell antibodies nor insulin-dependent diabetes mellitus developed during IFN alpha therapy, although hemoglobin-A1c levels were increased in 2 patients. One patient became positive for antimitochondrial antibodies, and another patient with preexisting antimitochondrial antibodies also manifested deterioration in liver function test results. Parietal cell antibodies and smooth muscle cell antibodies were the most frequent newly developed antibodies in 7 patients. Adrenal medullary cell antibodies and nuclear antibodies newly developed in 2 and 1 patients, respectively. At least 1 of 8 autoantibodies newly appeared in 19 patients (32.8%) and hypothyroidism developed in 2 patients (3.4%) during IFN alpha therapy. On the other hand, in 19 age- and sex-matched patients who did not receive IFN alpha, no autoantibody appeared, and no autoimmune disease developed during a follow-up period of 3 months. These findings suggest that IFN alpha acts as an immunomodulatory agent, inducing autoantibody production and the development of autoimmune disease in susceptible patients. Special attention should be paid to the development of hypothyroidism during IFN alpha therapy.
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PMID:Autoimmune endocrine disease induced by recombinant interferon-alpha therapy for chronic active type C hepatitis. 788 51

Recent evidence indicates that thyroid autoimmune disorders are associated with the presence of circulating autoantibodies (aAb) with dual specificity for thyroglobulin (TG) and thyroperoxidase (TPO). The question of whether these aAb, called TGPO aAb, are of clinical relevance compared to TG and TPO aAb remains to be determined. The availability of purified preparations of human TG and TPO allowed the development of a specific and sensitive RIA for TGPO aAb in serum. In the present study, we compared levels of aAb that cross-react with both TG and TPO (TGPO aAb) and total TG and TPO aAb levels, respectively, in sera from 84 normal controls and 226 patients with various thyroid and autoimmune diseases, including nontoxic goiter (n = 50), toxic nodular goiter (n = 13), thyroid carcinoma (n = 20), primary idiopathic myxedema (n = 15), postpartum thyroiditis (n = 11), Hashimoto's thyroiditis (n = 38), pernicious anemia (n = 27), rheumatoid arthritis (n = 19), and insulin-dependent diabetes mellitus (n = 33). In addition, 16 patients with Hashimoto's thyroiditis were studied before therapy and after more than 3 months of treatment with L-T4. It was shown that TGPO aAb were generally, but not always, present in the serum of patients with Hashimoto's thyroiditis, which also contained TG and TPO aAb. In contrast, TGPO aAb were undetectable in normal controls (excepting a few cases reaching borderline levels) as well as in sera from the majority of the other patients tested. Selecting sera positive for TGPO and either TG or TPO aAb, a statistically significant correlation was found between TGPO and TG (n = 26; P < 0.005), but not TPO aAb. Interestingly, the TGPO aAb level significantly decreased in patients with Hashimoto's thyroiditis after hormonal therapy (P < 0.05), some of them shifting from TGPO aAb positive before treatment to negative after treatment. In conclusion, TGPO aAb determination distinguishes Hashimoto's patients from patients with either thyroid and/or autoimmune diseases. The specific presence of TGPO aAb in a subset of Hashimoto's patients and their variation during T4 therapy remain to be understood. This could give a clue to mechanisms of autoimmune thyroid disease.
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PMID:Bispecific thyroglobulin and thyroperoxidase autoantibodies in patients with various thyroid and autoimmune diseases. 796 36

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