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

Insulin-dependent diabetes (IDDM) is frequently associated with autoimmune thyroid disease (ATD) within families. In these families, HLA polymorphism may modulate the susceptibility to each disease. Families with IDDM were further categorized as to the presence of ATD. IDDM-affected subjects from families without ATD were compared with subjects with ATD or with IDDM and ATD from IDDM/ATD families and with a control group. IDDM susceptibility in IDDM/ATD families was negatively associated with the presence of DQB1*0602 [relative risk (RR) = 0.038; P = 0.0001; corrected P (Pc) = 0.0005] and *0301 (RR = 0.3; P = 0.002; Pc = 0.01) and positively associated with the presence of DQB1*0201 (RR = 3.4; P = 0.0007; Pc = 0.0035) and *0302 (RR = 5; P = 0.0001; Pc = 0.0005), regardless of ATD. Compared with the IDDM-only group, the ATD-only group had an increased frequency of subjects with DQB1*0602 (RR = 0.14; P = 0.031), suggesting that the known IDDM-protective effect of this allele may be independent of susceptibility to ATD; however, this difference was not significant when the P value was correlated for the number of alleles tested. In these families, susceptibility to ATD was only associated with DQB1*0201 (RR = 5.71; P = 0.0043; Pc = 0.021). Among subjects with DQB1*0201, there was a weak negative association between the presence of DQB1*0302 on the second haplotype and Hashimoto's thyroiditis (RR = 0.237; P = 0.026; Pc > 0.05). We conclude that in IDDM/ATD families, IDDM-affected subjects are at risk for ATD, especially those carrying DQB1*0201. This risk may be influenced by the alleles carried on the second haplotype, with DQB1*0302 (or a closely linked gene) protecting from Hashimoto's thyroiditis and favoring Graves' disease.
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PMID:HLA-DQB1-associated susceptibility that distinguishes Hashimoto's thyroiditis from Graves' disease in type I diabetic patients. 815 15

Strategies for studying the genetics of autoimmune diseases have undergone a considerable evolution during the last years, especially due to molecular biology techniques and to systematic genome studies. Genetic factors account for 20 to 40% of the risk, and environmental elements play a major role. The major histocompatibility complex comprising HLA genes remains the immunogenetic system most studied and most closely associated with various autoimmune diseases. These associations are mainly observed with HLA class II genes polymorphisms; the precise knowledge of their structure has allowed to define HLA sequence polymorphisms which are themselves risk markers: specific combinations of HLA-DQA and DQB alleles in insulin-dependent diabetes mellitus or a given DR, DQ haplotype for multiple sclerosis. No strong association with HLA-DP has been demonstrated. In all cases the genes involved have a normal structure and the disease is secondary to the combination of a given set of genes with environmental factors. The present knowledge of insulin-dependent diabetes mellitus and multiple sclerosis genetics is rather advanced. Other genes of the HLA region might also be involved in the genetic susceptibility. Results about other immunogenetic systems (T cell receptor genes or heavy chain immunoglobulin genes) are still contradictory but no major gene for autoimmune susceptibility seems to exist in these regions; however autoimmune diseases are under polygenic control; susceptibility genes shared between different diseases often occurring within the same families (Graves' disease and insulin-dependent diabetes mellitus) and genes specific for a given disease (insulin gene region in diabetes) both exist. The present rapid progress in this area is due to the use of highly polymorphic markers randomly distributed across the genome (microsatellites being most informative) and that of animal models: the list of "candidate genes or regions" potentially involved in the genetics of autoimmune diseases is enlarging; the development of coordinated epidemiological studies of molecular genetics along with the sharing of biological resources between different teams allow to build up powerful informative studies which will confirm or refute those "candidates". However, once the list of genes involved is established their mechanism of action will still take time to elucidate.
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PMID:[Genetics of autoimmune diseases]. 817 58

Since Hirata et al. first reported a patient with insulin autoimmune syndrome in 1970, 197 cases have been reported in Japan as of December, 1992. The clinical profiles of these 197 cases were as follows; the peak age at onset was 60-69 years and peak duration of hypoglycemic attacks was more than 1 and less than 3 months. There was no gender difference in the peak age of onset or duration of hypoglycemic attacks. Approximately 82% of the IAS patients had spontaneous remission without any positive treatment. Before diagnosis of IAS, 43% of the patients with IAS had been taking medication; methimazole (MTZ) for Graves' disease, alpha-mercaptopropionyl glycine (MPG) for cataracts, liver disease or rheumatoid arthritis, or glutathione for liver disease, all of which are sulfhydryl compounds. After such sulfhydryl compounds were discontinued, the hypoglycemic attacks subsided. Three patients with IAS experienced recurrence of the hypoglycemic attacks after re-administration of MTZ and MPG, although 6 patients who developed IAS without exposure to any drug had recurrent attacks without exposure to any drug around 1 year after the first hypoglycemic attacks had stopped. Thus, hypoglycemia in IAS is mainly transient and the development of IAS may be related to sulfhydryl compounds.
Diabetes Res Clin Pract 1994 Jan
PMID:Insulin autoimmune syndrome (Hirata disease): clinical features and epidemiology in Japan. 820 Mar

The changes in normal endocrine physiology which accompany pregnancy result in changes in normal ranges of hormone levels and in specific changes in the course and management of endocrine diseases. This review presents information about the various endocrine diseases and their management in pregnant adolescents. Normal pituitary function during pregnancy is described as is the effect of pregnancy on pituitary tumors such as microadenomas and prolactinomas. The effects of bromocriptine therapy in cases where tumor enlargement occurs during pregnancy are tabulated. Methods of distinguishing placental growth hormone secretion and pituitary growth hormone secretion in patients with acromegaly are presented (with the note that acromegalic patients rarely become pregnant). TSH-secreting, gonadotropin, and nonsecreting tumors are rare in this age group, and there is no evidence that they enlarge during pregnancy. The discussion of the pituitary covers chronic hypopituitarism, Sheehan's Syndrome, lymphocytic hypophysitis, and diabetes insipidus. After reviewing normal changes in thyroid physiology during pregnancy, hyperthyroidism (usually due to Graves' disease), thyroid storm, and hypothyroidism are considered. The adrenal is the next subject, with a brief description of normal changes during pregnancy followed by comments on Cushing's Syndrome, adrenal insufficiency, congenital adrenal hyperplasia, and primary hyperaldosteronism. The symptoms, diagnosis, and treatment of pheochromocytomas, which are uncommon during pregnancy but are associated with high fetal and maternal mortality, are the next topics. After a review of changes in calcium metabolism during pregnancy and hypercalcemia, this report ends with a consideration of diabetes mellitus which includes alterations in maternal carbohydrate metabolism during pregnancy, effects of diabetes on the fetus, and management of insulin-dependent diabetes mellitus during pregnancy (the most likely type to be present in adolescents).
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PMID:Endocrine problems of adolescent pregnancy. 824 53

We report a case of 26-year-old woman with Graves' disease and idiopathic hypoparathyroidism diagnosed at 11 years of age, who subsequently developed insulin-dependent diabetes mellitus (IDDM) at 17 years of age. Treatment with antithyroid agents had failed to control her Graves' disease and her IDDM was unmanageable despite insulin therapy. Surgical intervention was carried out, resulting in an improvement of both her hyperthyroidism and IDDM. This case is the first report of polyglandular autoimmune (PGA) syndrome, presenting the association of IDDM, Graves' disease and idiopathic hypoparathyroidism.
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PMID:Insulin-dependent diabetes mellitus associated with Graves' disease and idiopathic hypoparathyroidism. 825 54

The occurrence of multiple endocrine autoimmunity with organ-specific autoantibodies is well known. In this study we evaluated the presence of competitive insulin autoantibodies (IAA) in immune and non-immune diseases of the thyroid, utilizing a sensitive and specific radiobinding assay. We studied 37 patients with Graves' disease, 44 patients with Hashimoto's thyroiditis, 11 patients with non-immune thyroid diseases and 30 normal controls. In 5/37 (13.5%), 7/44 (15.9%) patients with Graves' and Hashimoto's diseases, respectively, but in none of those with non-immune thyroid disease or of the controls, IAA levels exceeded our upper limit of normal range (50 nunits/ml) (P < 0.01). Positive IAA levels ranged between 50 and 123 nunits/ml with fluctuation of these levels over time. Islet cell antibodies were not detected in any of the patients and the controls in the study. No association was found between propylthiouracile treatment and level of IAA. In none of 10 IAA-positive patients was the early phase insulin secretion of the intravenous glucose tolerance test below 46 mu units/ml, and in 2 subjects repeated tests after 3 years showed conserved insulin secretion. In conclusion, our findings show that 15% of patients with autoimmune thyroid diseases, produce specific IAA which do not seem to reflect aggressive beta cell destruction.
Diabetes Res Clin Pract
PMID:Low titer, competitive insulin autoantibodies are spontaneously produced in autoimmune diseases of the thyroid. 826 17

Research exploring the relationship between psychological factors and the onset, exacerbation, and perpetuation of endocrine diseases has focused primarily on three diseases: diabetes mellitus (DM), Graves' disease, and Cushing's disease. There is insufficient evidence to support the position that psychological factors directly affect the onset of DM. Recent laboratory studies suggest that stress is associated with changes in glucose regulation in a subset of diabetic patients and that temperament and coping strategies influence glycemic control in diabetic children and adolescents. Relaxation training may improve blood glucose control in non-insulin-dependent DM patients. There is no good evidence that psychological characteristics affect the development and course of thyroid disorder or Cushing's disease. Recommendations are made for future research.
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PMID:Psychological factors affecting physical condition. Endocrine disease literature review. 842 87

Endocrine autoimmune disorders are mediated by T cell-dependent responses to organ-specific antigens, but the mechanisms initiating the process remain unknown. Lymphocytes which use the gamma delta heterodimer as T cell receptor (TCR) for antigen constitute a distinct subset of T cells whose function remains elusive. In order to investigate their possible involvement in endocrine autoimmunity we have determined the proportion of gamma delta T cells in the peripheral blood of 23 patients with type 1 (insulin-dependent) diabetes mellitus (type-1 DM) and 30 patients with autoimmune thyrotoxicosis (Graves' disease). T lymphocyte TCR expression was assessed by fluorescence-activated flow cytometry on peripheral blood mononuclear cells using MoAbs UCHT1 (CD3), TCR delta 1 (gamma delta TCR), WT31 and beta F1 (alpha beta TCR) and both the percentage of T cells expressing gamma delta and the ratio gamma delta/alpha beta were calculated. In the diabetic patients gamma delta cells were not significantly different from the control group (7.7 +/- 54% versus 8.0 +/- 5.5% of T cells, P NS). There was no relation between the proportion of gamma delta lymphocytes and the presence of islet cell antibodies (ICA) in the sera. The Graves' patients showed a tendency towards a higher proportion of gamma delta T lymphocytes than the controls (gamma delta/alpha beta ratios: 0.095 +/- 0.047 versus 0.063 +/- 0.022, P = 0.03). In 14 Graves' patients the number of gamma delta were measured in paired samples of peripheral and intrathyroidal lymphocytes, demonstrating an expansion of gamma delta within the thyroid glands (0.21 +/- 0.3 versus 0.095 +/- 0.047, P = 0.032). Immunohistochemical studies showed that gamma delta cells were scattered among the predominant alpha beta lymphocytes infiltrating the thyroid gland and that they account for 10% of intraepithelial lymphocytes. No relation was found between the increase of gamma delta lymphocytes and any clinical features.
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PMID:Gamma delta lymphocytes in endocrine autoimmunity: evidence of expansion in Graves' disease but not in type 1 diabetes. 848 15

Lymphocytes from patients with insulin-dependent diabetes mellitus (IDDM), a chronic autoimmune disease, have recently been shown to have decreased surface expression of MHC class I antigens. Since IDDM and other autoimmune diseases share a strong genetic association with MHC class II genes, which may in turn be linked to genes that affect MHC class I expression, we studied other autoimmune diseases to determine whether MHC class I expression is abnormal. Fresh PBLs were isolated from patients with IDDM, Hashimoto's thyroiditis, Graves' disease, systemic lupus erythematosis, rheumatoid arthritis, and Sjogren's syndrome. Nondiabetic and non-insulin-dependent diabetes mellitus patients served as controls. MHC class I expression was measured with a conformationally dependent monoclonal antibody, W6/32. Freshly prepared PBLs from the autoimmune diseases studied and the corresponding fresh EBV-transformed B cell lines had decreased MHC class I expression compared with PBLs from normal volunteers and non-insulin-dependent (nonautoimmune) diabetic patients. Only 3 of more than 180 donors without IDDM or other clinically recognized autoimmune disease had persistently decreased MHC class I expression; one patient was treated with immunosuppressive drugs, and subsequent screening of the other two patients revealed high titers of autoantibodies, revealing clinically occult autoimmunity. Patients with nonautoimmune inflammation (osteomyelitis or tuberculosis) had normal MHC class I expression. Autoimmune diseases are characterized by decreased expression of MHC class I on lymphocytes. MHC class I expression may be necessary for self-tolerance, and abnormalities in such expression may lead to autoimmunity.
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PMID:Defective major histocompatibility complex class I expression on lymphoid cells in autoimmunity. 848 90

The authors refer to a case report in which two rare clinical syndromes, the Tolosa Hunt Syndrome (THS) and the polyglandular auto-immune syndrome (PGA) co-exist in the same patient and make a detailed analysis of the literature regarding this kind of diseases. The THS is a rare clinical condition characterized by a painful ophthalmoplegia due to an involvement of the cranial nerves and of the sympathetic nerve-fibres going through the cavernous sinus and the superior orbit cavity. Nowadays the diagnosis of TSH is made by high resolution computerized tomography aimed at the cavernous sinus and the upper orbital cavity. This method allows to notice if at the basis of this syndrome there are vascular, neoplastic or inflammatory diseases or if, as in e case here presented, by exclusion, we must think of an inflammatory process with unknown pathogenesis. In this case report the patient under observation process to be affected by THS and also by auto-immune polyglandular syndrome type III, as she was affected by diabetes type I, Basedow disease and alopecia. The authors believe that an auto-immune mechanism can be at basis of the THS, and this fact has already been pointed out in the literature in two previous works. An important feature of this case report has been the definitive improvement of the symptoms by an antithyroid effect and, also, by an immune suppressor activity. The Authors hope that there will be reported a greater number of cases pointing to the coexistence of the THS with autoimmune diseases.
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PMID:[Tolosa Hunt syndrome and autoimmune polyglandular syndrome. A rare case report]. 853 98


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