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

Insulin- and anti-immunoglobulin-antibodies have been recently reported in pre-diabetic subjects: the former has been proposed as a predictive marker of Type I diabetes in non-diabetic-subjects. To evaluate the diabetes-related specificity of these antibodies, the presence of insulin autoantibodies, using a recently developed and highly sensitive competitive radioimmune assay, and of anti-immunoglobulin antibodies together with that of immune complexes and of other autoantibodies has been investigated in patients with organ- or non-organ-specific autoimmune diseases. One hundred and eleven serum samples were assayed from patients with Graves' disease, primary hypothyroidism, chronic autoimmune thyroiditis, Addison's disease, chronic autoimmune hepatitis, pernicious anemia, lupus erythematosus, and rheumatoid arthritis, together with 45 serum samples from normal subjects. From patients with autoimmune diseases, 32.4% of all sera revealed values of insulin autoantibodies above the limit of positivity (p less than 0.001); anti-immunoglobulin antibodies were present in 4.1% of patients (NS); immune complexes were found in 19.5% (NS) of all patients, but in 38% of patients with Graves' disease and chronic hepatitis (p less than 0.02). There was a trend for multiple autoantibody positivity to be associated with high levels of insulin autoantibodies (p less than 0.05). Thus, whereas contrary to expectation anti-immunoglobulin antibodies are not associated with non-diabetes-related autoimmune diseases, increased humoral immunoresponsiveness to endogenous insulin appears to be related to autoimmunity in general rather than restricted to Type I diabetes.
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PMID:Autoantibodies to insulin do appear in non-diabetic patients with autoimmune disorders: comparison with anti-immunoglobulin antibodies and other autoimmune phenomena. 218 33

Diabetes-prone BB Wistar rats were fed a modified AIN-76 diet providing the following amounts of iodine for 10 wk: 0.2 mg/kg diet (recommended amount); 1.0 mg/kg; 2.0 mg/kg; or 3.0 mg/kg. The thyroids were examined for gross and microscopic changes and sera were assayed for antibodies to triiodothyronine (T3), thyroxine (T4), and thyroglobulin (Tg). The body weights and food consumption of the rats fed 0.2 mg of iodine/kg were significantly lower than those of the animals fed higher amounts. Urinary iodine excretion reflected dietary intakes. The thyroids from animals fed 2.0 and 3.0 mg/kg were significantly (P less than 0.01) larger than those from animals fed 0.2 mg/kg. One rat fed 0.2 mg/kg and 2 rats in each group fed 2.0 and 3.0 mg/kg had extensive lymphocytic thyroiditis. Three rats fed 1.0 mg/kg, 6 fed 2.0 mg/kg and 6 fed 3.0 mg/kg had enlarged thyroids. Two rats fed 0.2 mg/kg, 2 fed 2.0 mg/kg and 6 fed 3.0 mg/kg had detectable Tg antibodies. These data suggest that high iodine intakes increase Tg antibodies, which may be associated with an increase in autoimmune thyroiditis in these animals.
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PMID:Effect of dietary iodine on autoimmune thyroiditis in the BB Wistar rats. 292 47

A model for the possible pathogenesis of insulin-dependent diabetes mellitus (IDDM) is presented. It is partly based on studies of autoimmune thyroiditis and founded on the idea that inappropriate class II molecule expression in insulin-producing beta-cells of pancreatic islets could cause an organ-specific autoimmune disorder. The model is supported by results of several IDDM case studies as well as by the critical evaluation of the known effects of various lymphokines and lymphotoxins on endocrine target tissues. The possible roles of islet capillary endothelial cells and islet cell antibodies in the pathogenesis of IDDM are discussed.
Diabetes Care
PMID:Pancreatic beta-cell damage. In search of novel pathogenetic factors. 314 41

The effect of T4 on the incidence of lymphocytic thyroiditis and on titers of antibodies to thyroglobulin and thyroid microsomal antigen was studied in BB/W rats that are prone to develop spontaneously autoimmune thyroiditis and diabetes. Thirty-three animals were separated in two groups. Rats in one group had 1 mg T4 per liter of drinking water, and the other group was given no T4. After 3-4 months of therapy the T4-treated group had a reduced production of antibody to thyroglobulin (p less than 0.05) and to microsomal antigen (p less than 0.005) and a significantly lower frequency of lymphocytic thyroiditis (p less than 0.05). Our data are consistent with previous findings in experimentally induced thyroiditis in rats and suggest that T4 has an immunosuppressive effect.
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PMID:The effect of thyroxine on spontaneous thyroiditis in BB/W rats. 320 67

We typed patient groups with type I diabetes (n = 78), Graves' disease (n = 81), goitrous autoimmune (n = 52), "silent" (n = 18) and postpartum thyroiditis (n = 15) for human leucocyte antigens (HLA) A, B, C, DR and DQ. The results were compared to those obtained from 256 healthy controls typed for HLA-A, -B, -C and 140 typed for -DR. All these 140 controls were genotyped. Previously described associations of DR3 (OR (odds ratio) = 2.68, p less than 0.005) and DR4 (OR = 3.26, p less than 0.0001) in type I diabetes is confirmed. In this series, however, HLA-DR3/DR4 heterozygotes were apparently at no greater risk for type I diabetes than DR3 or DR4 homozygotes. The relative risk conferred by DR3/DR4 heterozygotes (6.48) was less than that for DR3 homozygosity (2.8), suggesting a recessive major histocompatibility complex-related susceptibility to type I diabetes. Graves' disease was associated with DR3 (OR = 3.02, p less than 0.0005); the increased frequency of DR3 homozygotes in this series is consistent with recessive HLA-linked susceptibility to Graves' disease proposed on the basis of family data. Hashimoto's thyroiditis, on the other hand, was associated with HLA-DR4 (OR = 3.08, p less than 0.0001), the latter finding confirming our earlier report on 21 patients. The increase of HLA-DR4 in both post-partum and silent thyroiditis suggests that these conditions are immunogenetically related, and may well represent variants of chronic autoimmune thyroiditis.
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PMID:HLA and autoimmune endocrine disease 1985. 348 59

We investigated the serial changes in the plasma levels of anti-thyroglobulin antibody (ATA) by solid-phase enzyme immunoassay, thyroid hormones and blood glucose, since spontaneous occurring lymphocytic thyroiditis (LT) has been found in spontaneously diabetic Bio Breeding/Worcester (BB/W) rat. We also observed the correlation between these levels and histological findings in the thyroid gland. The incidence of diabetes was 0% in 5 week old rats (group A), 70% in 11 week old rats (group B), and 86% in 20 week old rats (group C), while LT was observed in 0% in group A, 20% in group B and 48% in group C. Although the incidence of both increased with age, there was no link between LT and diabetes. Plasma ATA levels were 91.4 +/- 28.5 (OD492 X 1,000, mean +/- SEM) in the control (14 week old Wistar Furth) rats. 49.5 +/- 15.4 in group A, 197.8 +/- 41.5 in group B, and 376.7 +/- 48.7 in group C, again showing a clear increase with age. In group C, the plasma levels of ATA in rats with LT were significantly higher than those without LT. In addition, 6 out of 11 rats without LT had abnormaly high ATA levels. In group C, the plasma levels of free 3,5,3'-triiodothyronine (FT3) and total thyroxine (TT4), and also the FT3/TT4 ratio were significantly lower and the plasma levels of blood glucose were higher than in the other groups. There was no difference between the plasma thyroid hormone levels in rats with LT and those without LT. These studies suggest that LT may occur independently of insulitis, namely diabetes, ATA levels and the incidence of LT increase with age, the site of ATA production may not be confined to the thyroid gland, and the derangement of glucose metabolism may be one of the factors in the decrease in plasma thyroid hormone. The BB/W rat is not only a useful animal model to use in exploring the pathogenesis of human insulin-dependent diabetes mellitus, but also spontaneous autoimmune thyroiditis.
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PMID:Spontaneous autoimmune thyroiditis in Bio Breeding/Worcester (BB/W) rat. 355 49

Viable rat islet cells were used to detect islet cell surface antibodies (ICSA) in the sera of diabetic and control patients. ICSA were present in almost all recent-onset insulin-dependent diabetics younger than 30 yr (15/16); their incidence in other diabetics (6/22) was also higher than in normal controls (1/18) or in patients with autoimmune thyroiditis (1/12). The varying specificity of the ICSA for the different islet cell types led to the recognition of class I sera, whose ICSA bind exclusively to B cells, class II sera, binding only to A and pancreatic polypeptide (PP) cells and class III sera, reacting with the three islet cell types but not with D cells. Most recent-onset insulin-dependent diabetics younger than 30 contained class I-ICSA, which is consistent with an autoimmune basis of their disease and with an involvement of surface antibodies in the B cell destruction. The presence of class II ICSA in three older diabetics and in one normal control raises the question whether autoimmune reactions against A and PP cells exist and are associated with a distinct entity in islet disease. It is concluded that the autoimmune form of diabetes mellitus represents a heterogeneous group, in which ICSA-positive patients can be distinguished on the basis of their ICSA-binding to one or more islet cell types. Three techniques can be used for the further identification of circulating ICSA, namely binding experiments with purified A or B cells, electron microscopical analysis of ICSA-binding islet cells purified by fluorescence-activated cell sorting, and the immunocytochemical characterization of ICSA-positive cells.
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PMID:Islet cell surface antibodies from insulin-dependent diabetics bind specifically to pancreatic B cells. 612 26

We describe a female patient with insulin-dependent diabetes mellitus and autoimmune thyroiditis. Transient hyperthyroidism developed in the postpartum period in two successive pregnancies, followed by temporary hypothyroidism with eventual full recovery. The clinical course was consistent with "silent thyroiditis" and the circumstantial evidence suggested that alterations in the antibody titers due to pregnancy may have been responsible for these episodes. This case study serves to emphasize that hyperthyroidism and hypothyroidism in the postpartum period may be transient, and this fact should be considered in therapeutic management of such a patient.
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PMID:Recurrent transient hyperthyroidism and hypothyroidism associated with pregnancy. 634 29

Diabetes mellitus not infrequently coexists with hypo- and hyperthyroidism. Hyperthyroidism aggravates glucose intolerance. A review of this phenomenon reveals multiple mechanisms, which include increased hexose intestinal absorption, decreased responsiveness to insulin, and increased glucose production. Conflicting results are obtained when circulating insulin level is measured in thyrotoxicosis. The role of glucagon and alpha-cell sensitivity is unclear. Diabetes mellitus influences the assessment of thyrotoxicosis by falsely decreasing the blood levels of thyroxine (T4) and triiodothyronine (T3) during severely uncontrolled hyperglycemia. Hypothyroidism is found in about 3% of patients with insulin-dependent diabetes mellitus (IDDM). Moreover, 13-20% of IDDM patients have elevated blood thyrotropin levels and anti-thyroid antibodies. Hypothyroidism per se seems to ameliorate hyperglycemia. A subtype of IDDM shares similar immunogenetic features with familial autoimmune thyroiditis. Studies of IDDM probands who show a high prevalence of circulating thyroid antibodies reveal the presence of such antibodies in their first-degree relatives. Circulating islet-cell antibodies, detected in a majority of IDDM patients at the onset of their disease, tend to persist only in those patients with coexistent polyendocrine autoimmune disease, including thyroiditis. Similar human leukocyte antigen (HLA) locus types are associated with thyroiditis and IDDM, namely HLA-Dr3 and -Dr4.
Diabetes Care
PMID:Diabetes mellitus and thyroid disease. 640 Jul 13

We studied the incidence of goiters and that of thyroid antibodies in 278 patients with diabetes mellitus, in whom six subjects with primary hypothyroidism were excluded, and measured their serum TSH concentrations. The incidence of goiters was 31.8%, and was higher in females than in males. The incidence of goiters in diabetics under the age of 40 was higher than that in subjects more than 40 years old, and the incidence of microsome antibodies and thyroglobulin antibodies were found to be 18.5% and 1.8%, respectively, in these two groups. The percentage of microsome antibodies was lower in diabetics between the ages of 40 and 60 than in diabetics under the age of 40 or over the age of 60. The incidence of goiters and microsome antibodies was not related to the treatment of diabetes mellitus. There was a significantly positive correlation between serum TSH concentration and age in diabetics with serum TSH levels less than 5 microU/ml. As a result, although the incidence of goiters in diabetics was found to decrease with age, the incidence of thyroid antibodies and serum TSH levels were found to increase. These findings suggest that it might be possible to observe atrophic autoimmune thyroiditis, sometimes resulting in subclinical hypothyroidism, in aged diabetics.
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PMID:Thyroid abnormalities in diabetes mellitus. 668 Apr 96


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