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)

We evaluated six patients in whom a diagnosis of Sheehan's syndrome had been made. The plasma levels of the following hormones were measured: basal thyroxine (T4), estradiol and cortisol; and also follicle-stimulating hormone (FSH), luteinizing hormone (LH), growth hormone (GH), thyrotropin (TSH), prolactin (PRL) and adrenocorticotropic hormone (ACTH), basally and after acute challenge with LH releasing hormone (LHRH), GRF (1-29)NH2 or insulin hypoglycemia, TSH releasing hormone (TRH) and lysine-8-vasopressin, respectively. Two patients underwent chronic LHRH stimulation by pulsatile subcutaneous administration with infusion pump. In 4 cases, computed tomography (CT) was performed although cranial X-ray study was normal. A severe and generalized pituitary involvement was found in all patients, 3 of whom had diabetes mellitus. Probably, more insidious cases go unnoticed. The presence of asymptomatic partial empty sella (ES) in all the CTs that were carried out raises the possibility that it is another evolutive feature of SS.
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PMID:[Relations between Sheehan's syndrome and empty sella turcica. A functional study apropos of 6 cases]. 217 69

We previously showed that for Singapore diabetics, a low prevalence of islet cell antibodies (ICA) and insulin autoantibodies (IAA) were observed, unlike the high prevalence rates in Caucasian populations. In this report, we have measured other autoimmune markers (thyroid autoantibodies, thyrotrophin [TSH] receptor antibodies, rheumatoid factor and anti-dsDNA antibodies) to assess the extent of autoimmunity in our newly diagnosed diabetes patients and those with long-standing diabetes. Results indicate that there is a raised prevalence of thyroid autoantibodies in diabetics compared to the general population. Thyroid autoantibodies occurred in 24.3% (28/115) of the patients; thyroid microsomal antibodies (16.5%, 19/115) was much higher than for thyroglobulin antibodies (1.7%, 2/115). Prevalence rates of thyroid autoantibodies were lower in diabetics who were newly diagnosed (21.6%, 11/51), compared to those with long-standing disease (25.5%, 14/55). Three patients (3/9) with gestational diabetes were also positive for thyroid autoantibodies. TSH receptor antibodies associated with Graves' disease, were found in two patients. However, they also had thyrotoxicosis. Five patients (4.3%, 5/115) were detected with rheumatoid factor, but were clinically asymptomatic. Anti-dsDNA antibodies were not detected in any of the subjects. The presentation of thyroid autoantibodies or rheumatoid factor with age did not coincide with diabetes-associated ICA and IAA. It may mean that inspite of prevalence of subclinical autoimmunity in diabetes, autoimmunity against beta-cell lesions is not associated with the overall autoimmune tendency in our diabetes.
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PMID:Humoral immune abnormalities in diabetes mellitus. 222 99

Thalidomide, a derivative of glutamic acid, has immunosuppressive effects and suppresses graft-vs-host disease in the rat and following bone marrow transplantation in man. It is effectively used in the treatment of erythema nodosum leprosum and has a potential therapeutic effect in a variety of autoimmune diseases. In view of these observations, we evaluated the effect of thalidomide on the incidence of spontaneous and iodine-induced lymphocytic thyroiditis and spontaneous insulin dependent diabetes mellitus in the BB/Wor rat. Thalidomide did not suppress the incidence of lymphocytic thyroiditis and serum anti-thyroglobulin antibodies or affect the serum concentrations of T4, T3 and TSH in this rat model. Thalidomide also did not affect the incidence of insulin dependent diabetes mellitus. In contrast to preliminary studies in man and rat demonstrating efficacy in the therapy of autoimmune diseases, thalidomide did not prevent or suppress autoimmune lymphocytic thyroiditis or insulin-dependent diabetes mellitus in the BB/Wor rat.
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PMID:Effect of thalidomide on the incidence of iodine-induced and spontaneous lymphocytic thyroiditis and spontaneous diabetes mellitus in the BB/Wor rat. 238 27

Previous studies have suggested that ciamexone, a 2-cyan-aziridine derivative, is a selective immunomodulatory agent with potential therapeutic application in a variety of autoimmune diseases. In the present study, the effects of ciamexone on autoimmune lymphocytic thyroiditis and diabetes mellitus were studied in the BB rat. The data suggest that, in this animal model, ciamexone does not affect the frequency of autoimmune diabetes or lymphocytic thyroiditis nor does it affect the serum TSH or T4 concentrations.
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PMID:The effect of ciamexone on lymphocytic thyroiditis and insulin-dependent diabetes mellitus in the BB/Wor rat. 239 79

Human monoclonal antibodies to human endocrine cells have been obtained following the generation of immunoglobulin-secreting interspecies lymphocyte hybridomas. Peripheral blood lymphocytes from an adult patient presenting with acute onset, Type I, diabetes mellitus were fused in vitro with mouse myeloma cells of the NS1 cell line. Initial selection of resulting hybridomas was made by their ability to proliferate in HAT medium. Those hybridomas secreting human immunoglobulins were identified by radioimmunoassay and, thereafter, cloned at frequent intervals to ensure continued antibody production. Human monoclonal antibodies selected in this manner are being employed to identify those epitopes which are common antigenic targets during initial stages of autoimmune-mediated diabetes mellitus and associated multiple endocrinopathies. Of these antibodies, one (HML 3.22) recognizes an epitope present on the human TSH receptor and a second (HML 3.21) identifies a component of thyroglobulin. The potential value of human monoclonal antibodies as probes for analyzing autoimmune-mediated endocrine diseases is discussed.
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PMID:Human monoclonal antibodies to thyroid antigens derived by hybridization of lymphocytes from a diabetic patient. 243 25

Amiodarone, an antiarrhythmic agent, is known to occasionally induce alterations in thyroid function because of its iodine content and ability to inhibit T4 5'-monodeiodination. We herein describe the drug-induced chemical hyperthyroidism in a diabetic patient with ventricular premature beats. A 46-year-old man with well controlled diabetes mellitus revealed neck swelling during a 4 months' treatment with amiodarone for his frequent occurrence of ventricular premature beats. Physical findings were unremarkable other than grade III diffuse struma. Routine laboratory studies were almost normal. The results of thyroid function studies showed hyperthyroidism, including increases in T4 and free T4, slight increases in T3 and free T3, a marked increase in reverse T3 and a decrease in 123I 24-h uptake. TSH was low and did not respond to TRH. Antithyroid antibodies and TSH receptor antibodies were negative. The findings of the thyroid biopsy were unremarkable except for a mild follicular hyperplasia. After cessation of the drug, T3 and free T3 were returned to normal within 2 weeks, T4 and free T4 within 2 months and reverse T3 after 6 months. These data suggest that the struma and chemical hyperthyroidism observed in our patient were induced by amiodarone treatment.
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PMID:[A case of chemical hyperthyroidism induced by antiarrhythmic agent amiodarone]. 245 31

Numerous studies indicate that an impaired hypothalamopituitary axis plays an important role in reproductive and thyroid disorders in diabetic humans and animal models. Yet, several questions about the pathogenesis of these diabetic complications have not been answered. To evaluate the basal secretion of single gonadotrophs and thyrotrophs in vitro, uncultured pituitary cells from control rats and 1-mo streptozocin-induced diabetic (STZ-D) rats were studied with a reverse hemolytic plaque assay and morphometry. After light-microscopy immunocytochemistry for gonadotropin and thyrotropin (TSH), we recorded the ratio of plaque-forming to non-plaque-forming cells. The area of plaques produced by luteinizing hormone (LH), follicle-stimulating hormone (FSH), and TSH cells and the area of plaque-forming and non-plaque-forming cells were clearly smaller in diabetic than control rats. The plaque area, however, was more severely reduced than the cell area. The percentage of LH-, FSH-, and TSH-immunoreactive plaque-forming cells was greatly decreased in diabetic compared with control animals. In conclusion, our findings demonstrate that the LH-, FSH-, and TSH-secreting cells of diabetic rats released less hormone and were less numerous than the corresponding cells of control rats. Thus, several pathogenetic mechanisms might be involved in reduced gonadotropin and TSH release at the cellular level: 1) anatomical lesions of organelles involved in glycoprotein hormone synthesis and secretion, possibly due to insulin deficiency; 2) decreased gonadotropin-releasing hormone (GnRH) and thyrotropin-releasing hormone (TRH) receptors on pituitary cells; 3) inadequate GnRH and TRH stimulation; 4) high plasma corticosterone levels; or 5) a combination of points 1-4.
Diabetes 1989 Oct
PMID:Reverse hemolytic plaque assay study of luteinizing and follicle-stimulating hormone and thyrotropin secretion in diabetic rat pituitary glands. 250 79

A new syndrome in two siblings with primordial birdheaded nanism, progressive ataxia, goiter, primary gonadal insufficiency and insulin resistant diabetes mellitus is presented. Plasma concentrations of TSH, PTH, LH, FSH, ACTH, glucagon and insulin all working through cell membrane receptors were elevated. A generalized cell membrane defect was suggested to be the pathophysiological abnormality in these patients.
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PMID:Primordial birdheaded nanism associated with progressive ataxia, early onset insulin resistant diabetes, goiter and primary gonadal insufficiency. A new syndrome. 266 2

In insulin-dependent diabetes mellitus (IDDM) several organ-specific autoantibodies are found in addition to pancreatic islet cell autoantibodies. In the present study we researched the presence of thyroid microsomal antibodies (anti-TMS) in 33 young patients with IDDM and evaluated contemporaneously their thyroid function. 5 patients (15.4%) are found with significant levels of circulating anti-TMS, among them 4 (12.1%) were also subclinical hypothyroid. However 6 other patients are found with mildly altered thyroid hormone pattern in absence of circulating anti-TMS. Basal and TRH-stimulated TSH were significantly higher, whereas serum FT4 was significantly lower, in patients with IDDM and circulating anti-TMS than in patients with IDDM but without anti-TMS. These observations indicate a significant incidence of mild or subclinical hypothyroidism in patients with IDDM and anti-TMS. Thus the screening for anti-TMS is recommended in all patients with IDDM, then thyroid hormone pattern of anti-TMS positive patients must be periodically followed.
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PMID:[Thyroid hormone anomalies in patients with insulin-dependent diabetes mellitus and circulating antithyroid microsomal antibodies]. 274 68

Streptozotocin diabetes in rats is associated with reduced function of the hypothalamo-pituitary-thyroid axis. The structure and hormone secretion of the thyroid and pituitary glands were studied in adult male rats 1 month after streptozotocin injection. The thyroid of diabetic rats was characterized by decreased follicle area and epithelial thickness. By electron microscopy, thyroid epithelial cells were characterized by flattened and almost empty rough endoplasmic reticulum cisternae, scanty exocytotic apical and endocytotic vesicles as well as degenerate mitochondria and rough endoplasmic reticulum. By immunohistochemistry, intracolloidal thyroglobulin and T3 as well as intraepithelial thyroglobulin were reduced. Electron microscopic and immunohistochemical analysis of pituitary glands showed that in diabetic rats thyrotrophs were mostly of type II, and the number of thyrotrophs (type I + type II) was greater than in controls. By radioimmunoassay (RIA), plasma T3, T4, and TSH levels were markedly reduced, and the TSH response to TRH was deficient in diabetic animals. The pituitary TSH concentration was increased, as expected from the morphological data. This study demonstrates severe structural changes in the thyroid and pituitary glands of diabetic rats which are accompanied by marked alterations of their secretory activity.
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PMID:Thyroid and pituitary secretory disorders in streptozotocin-diabetic rats are associated with severe structural changes of these glands. 288 60


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