Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004364 (autoimmune disease)
 24,845 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The role of thyroid hormone in renal hydrogen ion secretion remains largely unknown, and there is only limited information on renal acidification in hypothyroid patients. In the present study two of five adult male patients with untreated primary hypothyroidism and without clinical evidence of systemic autoimmune disease were unable to lower their urine pH appropriately after short duration acid-loading. Since, prior to acid-loading, their arterial blood gas values were within the normal range and urinary bicarbonate excretion was trival, the findings are consistent with the incomplete syndrome of distal renal tubular acidosis. Although the mechanism of this abnormality remains unknown, thyroxine deficiency per se may in part be responsible.
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PMID:Renal acidification in hypothyroid man. 1 Oct 53

It has been suggested that autoimmunity and genetic factors may play a specific role in the development of idiopathic hypoparathyroidism. We reported a case of idiopathic hypoparathyroidism complicated with chronic thyroiditis. The patient, a woman 40 years old, visited our clinic because of tetany of both hands and dizziness. She was of short stature with a round face. She also had a goiter, hypocalcemia, hyperphosphatemia and decreased parathyroidal function, but renal function was normal. Her TSH level was slightly high with a positive microsome test (x 1600), and the levels of thyroid hormones tended to be low. Based on Ellsworth-Howard test findings, a diagnosis of idiopathic hypoparathyroidism was made, with the complication of chronic thyroiditis confirmed by the thyroidal biopsy. Administration of l alpha-OH-D3 normalized the level of serum calcium. No special treatment was given for the chronic thyroiditis in order to observe its natural course. Her TSH returned to normal, and the level of thyroid hormones was increased to normal ranges. Tests were positive for anti-adrenal antibody and anti-gastric antibody. The complication of chronic thyroiditis, an autoimmune disease, and a positive finding for every antibody suggested the possible involvement of autoimmunity in the mechanism of development of idiopathic hypoparathyroidism. The administration of 1 alpha-OH-D3 resulted in an increase in the serum calcium level and also normalization of levels of TSH and thyroid hormones. Thus, it is likely that the elevation of the calcium ion or immunoregulation by active vitamin D may have induced the increase in thyroid hormone secretion.
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PMID:[A case of idiopathic hypoparathyroidism complicated with chronic thyroiditis]. 178 1

Graves' disease is an organ-specific autoimmune disorder. There is no universal agreement on the mechanism of Graves' disease, but the over-activity of the thyroid is due to an antibody capable of attaching to and activating the TSH receptor of follicular cells. There are other extrathyroidal features that are not caused either by this antibody or by hyperthyroidism. The clinical diagnosis is generally straightforward and can be confirmed by in vitro measurement of thyroid hormones and TSH. A measurement of radioiodine uptake is also valuable. Treatment is not specific for the immunologic defect, but its purpose is to lower the thyroid hormone levels to normal. This can be achieved with antithyroid medication, radioiodine iodine-131, or thyroidectomy. In most clinical situations, a strong argument can be made for iodine-131 therapy, which is safe and definitive, although posttreatment hypothyroidism and the need for lifelong thyroxine are to be expected.
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PMID:Graves' disease. Current concepts. 198 48

Organ specific autoimmune diseases are relatively common immunological disorders in man which include thyroid autoimmune disease, insulin-dependent diabetes mellitus and myasthenia gravis. The target autoantigens in some of these diseases have recently been characterised. In thyroid autoimmune disease this includes the key enzyme, thyroid peroxidase (TPO), which is involved in the generation of thyroid hormone. Structural knowledge about autoantigens such as thyroid peroxidase will allow a greater understanding of the interaction between autoantigens and the aberrant immune response, and facilitate the development of strategies for antigen-specific therapeutic manipulation. We report here a prediction of the secondary structure of thyroid peroxidase, together with the results of circular dichroic spectroscopy of a homologous purified enzyme. A combination of 3 secondary structure prediction programs has been used, following multiple sequence alignment, and TPO has been found to consist mainly of alpha-helical conformation, with little beta-sheet present. This structure prediction, together with knowledge of the exon-intron boundaries allows a model for the domain organisation of the TPO molecule to be proposed.
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PMID:Prediction of domain organisation and secondary structure of thyroid peroxidase, a human autoantigen involved in destructive thyroiditis. 216 85

In this review, the major types of immune mediated thyroiditis are described and the etiology explained in the light of current theories of autoimmunity. Hashimoto's thyroiditis is a common autoimmune disease. The onset is gradual with patients presenting with symptoms of hypothyroidism, nonspecific symptoms of the autoimmune process itself, or symptoms relating to a goitre. The disease is usually relentless and, except in young patients, permanent replacement with thyroxine is eventually required. Silent thyroiditis is another autoimmune disease of more acute onset. The initial, thyrotoxic, phase lasting several weeks is due to release of thyroid hormone from damaged follicles, and radionuclidic scans show absent uptake. There often follows a hypothyroid phase with final recovery in most patients. Post partum thyroiditis is due to silent thyroiditis, or, less commonly, Hashimoto's thyroiditis, occurring three to six months after delivery. Subacute thyroiditis often follows a viral infection and is not thought to be an autoimmune disease. It presents with severe thyroid pain and tenderness with marked non-specific symptoms such as myalgia and fatigue. The initial, thyrotoxic, phase is also due to release of thyroid hormone, and radionuclidic scans show absent uptake. A hypothyroid phase often follows and recovery is complete. Hashimoto's thyroiditis appears to be due to a congenitally present, antigen specific, T suppressor lymphocyte defect. It is proposed that in silent thyroiditis there is a less severe Ts defect and a correspondingly greater decompensating factor. In post partum thyroiditis, this factor appears to be a general decline in T suppressor lymphocyte function after delivery. Subacute thyroiditis is not an autoimmune disease. The thyroid appears to be an "innocent bystander" in an immune mediated antiviral attack.
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PMID:Thyroiditis. 293 21

We examined basal and bTSH-stimulated human thyroglobulin (hTg) secretion by autologous normal and abnormal (benign and malignant) human thyroid cell monolayers. Basal and bTSH-stimulated hTg secretion was highly variable and ranged from 50-700 ng/ml/10(5) cells over a 6 day period. All normal and benign 'non-functioning' adenoma cells demonstrated a dose and time related stimulation of hTg secretion in response to bTSH. Comparison of hTG secretion by autologous normal and abnormal cells showed that in six of eight pairs, the normal thyroid cells had a greater output of hTg than the benign adenoma cells in contrast to our previous studies using non-autologous cells. Malignant thyroid cell hTg production was less predictable than that obtained with normal and benign thyroid cells varying from absent to normal responses to bTSH. Characterization studies of the secreted hTg showed no difference between normal, benign and malignant thyroid cell hTg with reference to molecular weight. However, hTg secreted in vitro was non-iodinated and had a marked reduction (up to 200-fold) in immunoreactivity assessed by both polyclonal and monoclonal antibodies to hTg when compared to hTg standard prepared from intact thyroid tissue (which had 4.58 micrograms iodine/mg). This reduction in hTg immunoreactivity was greatest for hTg secreted by malignant thyroid cells. These data demonstrate the wide variability in the hTg secretory capacity of human thyroid cell monolayers and indicate, when compared to autologous normal cells, that abnormal human thyroid epithelial cells may be relatively deficient in their ability to secrete hTg in vitro. There were also qualitative differences in the immunoreactivity, and iodine content, of in-vitro secreted hTg. These observations suggest that there may be much greater heterogeneity in hTg secreted in vitro than previously realized, perhaps secondary to differences in iodine content and/or degree of glycosylation. Human thyroglobulin (hTg) is the major secretory protein of the thyroid cell (Van Herle et al., 1979). Intracellular hTg is the site of thyroid hormone iodination yet its extrathyroidal role, if any, remains unclear. While hTg is usually present in the peripheral circulation of normal individuals, in species of differing molecular weight (Feldt-Rasmussen et al., 1978), there have been few studies of in-vitro production of hTg by isolated human thyroid cells. Our interest in hTg is in its role as an antigen in thyroid autoimmune disease (De Bernardo et al., 1983; 1986).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Variability in production and immunoreactivity of in-vitro secreted human thyroglobulin. 345 72

The present report summarizes experiments with monoclonal antibodies to the TSH receptor. The data provide further insight into the TSH receptor structure and into the basis of autoimmune antibodies implicated in the pathogenesis of Graves' disease. They resolve many clinical questions and provide new approaches to enhance our understanding of autoimmune disease. In one new approach, it has been noted that the 11E8 TBIAb can precipitate the phosphorylated beta subunit of the insulin and IGF1 receptor. This cross-reactivity or recognition of determinants adjacent to the TSH receptor may not be random. Insulin, IGF1, alpha 1 adrenergic, and TSH receptors have been linked to a synergistic cascade response system of the thyroid involving growth, thyroglobulin biosynthesis, iodination of thyroglobulin, and thyroid hormone formation. Future studies with the monoclonals may help unravel this cascade system and its regulatory relationships, along with the relationships between autoimmune thyroid disease and autoimmune diseases of other organs.
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PMID:Monoclonal antibody studies defining the origin and properties of autoantibodies in Graves' disease. 349 61

Hypothyroidism is commonly thought to cause decreased gastric emptying and secretion, but these may be related to associated autoimmune disease or chronic changes. Therefore, we measured gastric emptying and secretion in 11 healthy controls and in nine patients (19-54 years old; five females and 4 males) rendered athyreotic by surgery and/or 131I for thyroid cancer. Replacement T4 was stopped 47-65 days and subsequent replacement T3 was stopped 33-40 days before the study. All patients were symptomatic with complaints including weight gain, lethargy, and constipation. Deep tendon reflexes had delayed relaxation phase. Serum cholesterol and creatine phosphokinase levels were elevated. Thyroid hormone levels were markedly decreased (means +/- SE; T4: 0.7 +/- 0.3 micrograms/dl; free T4: 0.2 +/- 0.1 ng/dl; T3: 28 +/- 6 ng/dl) and TSH was markedly increased (88 +/- 16 microU/ml). Gastric fractional emptying rate (%/min) and hydrogen ion (H+) output (meq/hr) were determined before and following two sequential stimulations: a 250-ml water load and an intravenous infusion of pentagastrin (6 micrograms/kg/hr). There were no significant differences between controls and athyreotic patients. Our data demonstrated that short-term, profound, thyroid hormone deficiency does not modify gastric emptying or acid output.
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PMID:Gastric secretion and emptying in hypothyroidism. 671 56

The aim of this study is to determine whether antithyroid drugs (ATD) act via inhibiting thyroid hormone synthesis or by interfering with the immune process which leads to autoimmune disease. Previously we had demonstrated that ATD do not affect HLA-DR and TPO antigen expressions induced by appropriate stimulus in normal thyrocytes, so we decided to study what happens when the same experiments are performed using autoimmune thyrocytes. Cultured thyroid tissue from patients operated on for Graves' Disease or Hashimoto's Thyroiditis were stimulated with TSH or TBII alone or associated with ATD; TPO antigen expression was evaluated by the Cytotoxicity Assay using human monoclonal antiTPO. When autoimmune thyrocytes were cultured and no stimulus was used or with the addition of MMI or PTU alone, very low values of TPO expression were noted (8.6 +/- 6.7, 5.0 +/- 7.1 and 4.2% +/- 2.3% respectively); if they were stimulated with TSH or TBII, a sharp rise of TPO antigen expression was detected (54.4 +/- 23.3 and 62.6 +/- 16.5%), these figures being significantly different from unstimulated cells (p < 0.001). If both stimulus were used associated with ATD, the high TPO antigen expression was unaffected. It is concluded that, at least in vitro, ATD have no effect upon induced-antigen expression in autoimmune thyrocytes. Since they do not alter antigen presentation, a primary step in the immune process, it is difficult to accept that their mechanism of action is through interference with the immune response.
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PMID:[Lack of in vitro effect of antithyroid drugs upon peroxidase antigen expression in autoimmune thyroid disease]. 751 5

An association between insulin-dependent diabetes mellitus (type 1) and thyroid diseases has long been reported, but the morphological evaluation of the thyroid in type 1 diabetes patients without overt thyroid disease has always been limited to physical examination. Ultrasonography of the thyroid gland was performed in 45 patients with type 1 diabetes without overt thyroid disease, to study thyroid volume and the prevalence of thyroid nodules. Data were compared with those obtained in 45 age- and sex-matched control subjects residing in the same area. In the patients, thyroid volume had increased on average by 46%; 35% of male and 32% of female patients had a thyroid volume exceeding the 95% confidence limits of the matched controls. The prevalence of thyroid nodules was only slightly raised. On average, free thyroxine was increased in the presence of normal triiodothyronine levels. Four patients were frankly hyperthyroid. The patients also showed a higher prevalence of thyroid-microsomal antibodies, but the thyroid hormone status was not different in relation to thyroid volume, nor was thyroid volume in relation to the presence of autoantibodies. Patients with type 1 diabetes without overt thyroid disorders may have morphological, ultrasonographically detectable alterations of the thyroid gland, the expression of a possible involvement of the thyroid in an autoimmune disorder not limited to the islet cells.
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PMID:Thyroid volume in type 1 diabetes patients without overt thyroid disease. 761 18


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