Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Islet cell antibodies (ICA-IgG and complement-fixing-ICA), parietal cell antibodies (PCA), intestinal epithelial cell antibodies (IECA), thyroglobulin (TgA) and thyroid microsomal antibodies (MsA), antinuclear (ANA) and reticulin antibodies (RA), were studied in 55 insulin-dependent diabetic patients (30 males and 25 females), aged 2-19 years with diabetes from a few days up to 14 years. In 58% of the diabetics one or more autoantibodies were found: ICA-IgG (31%), CF-ICA (16%), PCA (34%), TgA (9%), MsA (9%), ANA (13%), RA (2%). Autoantibodies were significantly more frequent in females (76%) than in males (43%) (P less than 0.025). ICA-IgG, CF-ICA, PCA, ANA were significantly more frequent in patients than in controls. The frequency of ICA-IgG and CF-ICA was significantly higher during the first 3 years of disease than afterwards (P less than 0.001); a similar pattern was observed for PCA, TgA, MsA. Of the 87 parents and 30 siblings screened for ICA-IgG, CF-ICA, PCA, IECA, TgA, MsA, ANA and RA, 42 (44%) had one or more autoantibodies, which were more frequent in females than in males. Seven relatives (6%) were ICA-IgG positive (four mothers, two fathers and one brother), and only one mother, ICA-IgG negative, was CF-ICA positive. Other autoantibodies were also more frequent in parents than in controls. Autoantibody-positive relatives have been asymptomatic up to now.
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PMID:Auto-immunity in children with diabetes mellitus and in their relatives. 376 71

Thyroid autoantibodies are common in Type 1 diabetics and their first degree relatives and may be part of the autoimmune diathesis present within such families. We have measured the prevalence of microsomal (M-Ab) and thyroglobulin (Tg-Ab) autoantibodies in 84 HLA-typed families having a Type 1 diabetic child, using enzyme-linked immunosorbent assay techniques. Thyroid autoantibodies were detectable in 201/407 (49%) individuals in these families. Both autoantibodies were significantly more frequent in the subsets of parents, diabetic children and their non-diabetic siblings than in groups of control adults and children. The prevalence of these autoantibodies in the diabetic families was increased in both sexes with a female:male ratio of 1.4:1. Antigen DR5 was significantly associated with M-Ab production but only for male subjects (P = 0.005 after correction for the number of DR antigens tested). No significant associations were encountered for Tg-Ab. Within-family analyses indicated that thyroid autoantibodies occurred with increased prevalence in HLA-identical or haplo-identical siblings of autoantibody-positive index cases in comparison to control children. We conclude the DR association with thyroid autoantibody production in this diabetes-selected population was thyroiditis-related and not diabetes-related, and the DR5 association was restricted to males and the production of M-Ab. These data are consistent with the hypothesis that multiple genetic and non-genetic factors played a role in the high prevalence of thyroid autoantibodies in this population.
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PMID:Thyroid autoantibodies in HLA-genotyped type 1 diabetic families: sex-limited DR5 association with thyroid microsomal antibody. 379 56

In most of the cases, once a given endocrine gland is involved, the corresponding specific autoantibody may be detected; for example, anti-islet cell antibodies are produced within the first few years, after onset of symptoms in insulin-dependent diabetes (DID). Accompanying autoantibodies are quite frequently found in the patient himself. In Schmidt's syndrome (thyroid and adrenal glands are involved and associated to IDD in 30% of the cases) thyroid microsomal antibodies are found in 38% of the cases, thyroglobulin antibodies in 11% of the cases, islet-cell antibodies in 7% of the cases and steroid cell antibodies in 17% of the cases. Associations are also possible in patient family members. Aberrant expression of HLA-DR molecules at the membrane of follicular thyroid cells (as of any other endocrine gland), following a viral aggression, could well account for the endocrinopathy combinations, but alternative mechanisms should be discussed.
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PMID:[Autoimmune polyendocrinopathies. Pathogenic hypotheses]. 382 97

A 37 year old male with a strong family history of autoimmune disease presented with typical symptoms of hyperthyroidism. He had exophthalmos but no goitre. Hyperthyroidism was confirmed by failure of 131I neck uptake to suppress after 7 days treatment with triiodothyronine. Six years previously a diagnosis of primary hypothyroidism has been made. At diagnosis of hyperthyroidism, thyroglobulin antibodies, thyroidal microsomal antibodies and thyroid stimulating immunoglobulins were detected. The absence of thyroid growth stimulating immunoglobulins and presence of immunoglobulins blocking TSH-induced growth may account for the absence of goitre throughout. HLA -B8, -B, -DR3 and -DR4 genotypes, low C4 complement concentrations and islet cell autoantibodies were detected at the time of diagnosis and 1 year later diabetes mellitus developed.
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PMID:Hyperthyroidism following primary hypothyroidism in association with polyendocrine autoimmunity. 388 26

The effect of diabetes mellitus on the synthesis and secretion of thyroid hormone ws investigated in mice with streptozotocin-induced diabetes. Thyroid glands were labeled in vivo with 131I for 2 h. In control animals, TSH stimulated the synthesis of PB127I and 131I-labeled iodothyronines and simultaneously decreased the proportion of 131I-. These effects of TSH were not observed in diabetic animals but were demonstrable in diabetic animals treated with insulin. For studies of hormone secretion, labeled thyroid glands were cultured in vitro in medium containing 1 mM mononitrotyrosine. The rate of the hydrolysis of labeled thyroglobulin was measured as the proportion of 131I-labeled iodotyrosines and 131I-labeled iodothyronines recovered at the end of culture and was used as an index of thyroid secretion. TSH in vivo stimulated the rate of thyroglobulin hydrolysis for 6 h, with a peak occurring after 2 h. The diabetic mice had a diminished response to TSH, which improved on treatment with insulin. The addition of TSH and insulin to the culture medium significantly increased the rate of thyroglobulin hydrolysis in glands of diabetic mice over that resulting from the addition of dibutyryl cAMP alone. The generation of thyroidal cAMP in response to TSH was higher in diabetic mice than in controls. The rise in plasma T4 and T3 2 h after the administration of TSH was less in diabetic mice than in control mice or diabetic mice treated with insulin. Our studies, therefore, indicate that the thyroidal response to TSH is decreased in diabetes mellitus. The defect appears to be at a step beyond the generation of cAMP.
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PMID:Decreased thyroidal response to thyrotropin in diabetic mice. 627 30

For 4 to 8 years we followed up 3 diabetic patients in whom the onset of diabetes seemed to be closely related to the well-documented Epstein-Barr virus infection (Case 1) or Coxsackie B4 virus infection (Case 2, 3). Although all developed acute ketosis-prone diabetes in the convalescent stage of the viral infections, the subsequent clinical courses were quite different from each other. Case 1 has remained consistently insulin-dependent and associated with positive islet cell antibody, gastric parietal cell antibody, thyroglobulin hemoagglutinating antibody and thyroidal microsomal hemoagglutinating antibody. Case 2 restored normal glucose tolerance. Case 3 has become noninsulin-dependent diabetes mellitus after a 6 year interval. Thus, it is reasonably presumed that virus could be responsible for the occurrence of different phenotypes of diabetes.
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PMID:Various phenotypes of diabetes mellitus at ultimate outcome of acutely developed diabetic state induced by viral infection. 628 96

An increased prevalence of Type 1 (insulin-dependent) diabetes has been reported in patients with congenital rubella. Rubella virus multiplies in the pancreas, and we have hypothesized that studies of children with congenital rubella would be of great importance in following the development of Type 1 diabetes in a defined, susceptible population. Two hundred and forty-one children with congenital rubella (mean age 17.4 +/- 0.3 years; 65% black and hispanic) have been evaluated, 30 of whom already have diabetes and 17 of whom have borderline glucose tolerance. In these latter two groups, HLA-DR3 is significantly increased and HLA-DR2 significantly decreased. Pancreatic islet cell cytotoxic surface antibodies are found in 20% of the total congenital rubella population, including in more than 50% in the time period before they develop diabetes and are not related to any specific HLA type. In addition, anti-microsomal and anti-thyroglobulin antibodies are found in 34% of this population. The data demonstrate that Type 1 diabetes developing in congenital rubella patients has the genetic and immunological features of classical Type 1 diabetes, namely the presence of HLA-DR3, the absence of HLA-DR2, islet cell surface antibodies before decompensation and an increased prevalence of anti-thyroid antibodies. Patients with non-diabetic congenital rubella represent an easily identifiable group in whom other immunological factors associated with Type 1 diabetes can be elucidated and possibly modified.
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PMID:Congenital rubella syndrome as a model for type 1 (insulin-dependent) diabetes mellitus: increased prevalence of islet cell surface antibodies. 638 25

A solid-phase immunosorbent radioassay for the detection of circulating antibodies to protein hormones is described. The assay is based on the binding of the homologous 125I-labelled antigen to the antibodies which are then bound to anti-IgG antibodies covalently coupled to Sepharose. It can easily be applied as a complement to any radioimmunoassay for the detection of circulating antibodies to the ligand measured. The assay system avoids falsely elevated values due to interference of high serum concentrations of the antigen. The assay was applied to measure antibodies to FSH, LH, TSH, GH, prolactin, insulin and thyroglobulin (Tg). Among patients with chronic thyroiditis Tg antibodies were found in 100% of the sera. In diffuse toxic goitre 73% of the patients had detectable Tg antibodies. Insulin antibodies were present in 82% of the sera from patients with insulin treated diabetes. No antibodies were found against the other protein hormones tested.
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PMID:A new sensitive immunosorbent radioassay for the detection of circulating antibodies to polypeptide hormones and proteins. 643 35

Serum thyroglobulin (Tg) was measured in the cord blood of 635 newborns and serum thyroxine (T4) reverse triiodothyronine (rT3), TSH and T3 were measured in about 200 of them. Cord Tg was detectable in all newborns with a mean +/- SE value (50 +/- 1.3 ng/ml) higher than that found in the serum of adult subjects (n = 144; Tg = 13 +/- 1.1; p less than 0.0001). Cord Tg had a log-normal distribution. A low, but positive correlation was found between cord Tg and cord TSH (n = 242; r = 0.17; p less than 0.05) but not with cord T4 or cord rT3. Gestational age was negatively correlated with cord Tg or cord rT3 (rS = 0.97; p less than 0.01; rS = -0.89; p less than 0.02, respectively) while was positively correlated with cord T4 or cord TSH (rS = 0.85; p less than 0.05; rS = 0.86; p less than 0.01, respectively). Birth weight, maternal diabetes, induction of labor with oxitocin, cesarian section and newborns' illness showed no influence on cord Tg levels when considered alone, but decreased cord Tg levels were found in ill newborns delivered by cesarian section. On the contrary, increased cord Tg levels were present in cord blood of newborns who developed hypoglycemia soon after birth and in small for gestational age newborns. In 24 newborns studied daily for the first 6 days of life, serum Tg was always detectable with mean values not different from those found in the cord blood.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum thyroglobulin in newborns' cord blood, in childhood and adolescence: a physiological indicator of thyroidal status. 651 82

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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