Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of 3 units of thyrotropic hormone to rabbits with autoimmune thyroiditis and hypothyroidism led to reduction of the I131 absorption by the thyroid gland and to increase in the activity of proteolytic enzymes of the gland. Apparently, in autoimmune thyroiditis disturbances at the stages of the iodide incorporation into the gland were irreversible; proteolysis depression was apparently secondary. Possibly the mentioned disturbances were associated with the circulating antithyroid antibodies.
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PMID:[The effect of thyrotropic hormone on processes mediating the cytotoxicity of antithyroid antibodies]. 93 90

Polymyalgia rheumatica developed in a 71-year-old patient within 2 years of the onset of acute sarcoidosis with biopsy-verified involvement of the thyroid, and concomitant autoimmune thyroiditis with hyperthyroid symptoms. Three years after the onset of muscle symptoms a non-metastasizing breast carcinoma was discovered and treated surgically. Neither the long interval between the onset of polymyalgia rheumatica and the discovery of the breast tumour, nor the good response of muscle symptoms to a one-year maintenance treatment with corticosteroids, was consistent with a paraneoplastic mechanism of the polymyalgia rheumatica syndrome. It was therefore hypothesized that the various disorders suffered by this patient might be related to a partly age-dependent depression of T-lymphocyte function, leading to an altered immunological reactivity to which the various clinical manifestations could be attributed. Such a hypothesis is supported by recent reports showing that in old people and in ageing experimental animals, a decrease in T-lymphocyte function and in the number of circulating T-cells occurs concomitantly with an increase in the incidence of a variety of neoplasms and autoimmune disorders.
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PMID:Sarcoidosis with thyroid involvement, polymyalgia rheumatica and breast carcinoma. A case report. 93 26

We present the case of a 63 years old man (177 cm height, 111 kg weight) with autoimmune thyroiditis. He had a long term history of hypersomnolence and heavy snoring. Two years ago, because of a bifascicular block and sinus pauses, a cardiac pace-maker was placed. Polysomnography recording showed a systematic periodic breathing characterized by profound desaturation waves (often 92% Sa O2 to 60% Sa O2) every 60 seconds, secondary to prolonged mixed apneas. Hormone replacement therapy and a 17 kg weight loss completely suppressed the sleep apnea syndrome within five months. We conclude that SAS is a major component of the respiratory depression in hypothyroidism and that normalisation of thyroid function can definitely cure the patient.
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PMID:[Sleep apnea syndrome and hypothyroidism: apropos of a new case and a review of the literature]. 265 40

Considerable research over the past 20 years has documented alterations in the hypothalamic-pituitary-thyroid (HPT) and hypothalamic-pituitary-adrenal (HPA) axes in patients with affective disorders, especially depression. Although plasma concentrations of thyroid hormones (T3, T4) are generally unaltered in patients with major depression, plasma thyroid stimulating hormone (TSH) responses after intravenous administration of thyrotropin-releasing hormone (TRH) are blunted in approximately 25% and abnormally elevated in approximately 15% of depressed patients. Data are presented supporting the hypothesis that TSH blunting may be secondary to central nervous system (CNS) hypersecretion of TRH, and that the enhanced TSH response may be secondary to subclinical hypothyroidism associated with autoimmune thyroiditis. The HPA axis has received considerable scrutiny in depressed patients and there is universal agreement that 50% to 75% of patients with major depression exhibit hyperactivity of the HPA axis characterized by hypercortisolemia, ACTH hypersecretion, and nonsuppression of plasma cortisol concentrations after administration of the synthetic glucocorticoid dexamethasone. Evidence is presented that hypersecretion of corticotropin-releasing factor (CRF) contributes, at least in part, to HPA axis hyperactivity and perhaps to certain of the signs and symptoms of major depression.
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PMID:Clinical significance of psychoneuroendocrinology in psychiatry: focus on the thyroid and adrenal. 265 28

The role of T lymphocytes in the pathogenesis of experimental autoimmune thyroiditis in mice is well established while the role of B lymphocytes is unclear. Mice with thyroid lesions have thyroglobulin antibodies whereas these antibodies can occur in mice immunized with Tg that do not develop thyroid lesions. To determine whether thyroglobulin antibodies are necessary for the development of the thyroid infiltrates with mononuclear cells, which are characteristic for experimental autoimmune thyroiditis, AKR mice chronically treated from birth with goat anti-mouse IgM antibodies were immunized with mouse thyroglobulin in Freund's complete adjuvant when they were 7 weeks old. Control mice, similarly immunized, were chronically injected from birth with normal goat gamma-globulin. Three weeks after immunization, all mice were sacrificed, thyroglobulin antibodies in the serum were measured by hemagglutination assay and enzyme-linked immunosorbent assay, and thyroid pathology was assessed. The serum concentration of IgG and IgM, the percentage of B and T lymphocytes in the spleen (flow cytometry), and the in vitro proliferative response of spleen lymphocytes to stimulation by PHA, LPS, and Tg were also measured. All mice treated with anti-IgM antibodies did not have detectable thyroglobulin antibodies but 63% of these mice and 88% of control mice (all of which had thyroglobulin antibodies) had thyroid lesions. Mice treated with anti-IgM antibodies that did not have thyroid lesions had a more pronounced depression of B lymphocytes than similarly treated mice that had thyroid lesions. These experiments suggest that thyroglobulin antibodies are not necessary for the development of thyroid infiltrates with mononuclear cells. B lymphocytes could still participate in the production of experimental autoimmune thyroiditis by presenting thyroglobulin to helper T lymphocytes.
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PMID:Experimental autoimmune thyroiditis in mice chronically treated from birth with anti-IgM antibodies. 278 67

Contrary to reports on depression, the prevalence of antithyroid antibodies was not significantly higher in 38 patients with panic disorder than in 38 matched control subjects. Autoimmune thyroiditis is not commonly associated with panic disorder but may play a role in some specific clinical circumstances.
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PMID:Autoimmune thyroiditis and panic disorder. 291 71

The magnitude of the thyroid-stimulating hormone (TSH) response induced by thyrotropin-releasing hormone (TRH) helps identify patients whose thyroid is failing. Many of these patients have been found to have Hashimoto's thyroiditis, symptomless autoimmune thyroiditis (SAT), and subclinical hypothyroidism. While patients with SAT are clinically euthyroid, what might be "symptomless" for the endocrinologist might be a syndrome presenting with psychiatric symptoms to the psychiatrist. As a preliminary test of this hypothesis, we tested 100 consecutive admissions to a psychiatric hospital who complained of depression or lack of energy. Fifteen (15%) of 100 patients were identified from the baseline thyroxin (T4), triiodothyronine (T3) resin uptake (RU), T3 radioimmunoassay (T3RIA), TSH, and TRH test who met criteria for either subclinical, mild, or overt hypothyroidism. Of these 15 patients, 9 (60%) had positive thyroid microsomal antibodies with titers of greater than or equal to 1:10. Our data suggest that SAT is not symptomless and may be an important diagnosis to consider in the evaluation of depressed, anergic, or atypical patients.
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PMID:"Symptomless" autoimmune thyroiditis in depression. 681 Apr 1

Impairment of cognitive function can occur with thyroid disorder and also with depression. Since depression occurs in conjunction with postpartum autoimmune thyroiditis, the question arises as to whether any impairment of cognitive function in postpartum women is related to change in thyroid status or to depressed mood. A total of 242 women (110 thyroid antibody-positive and 132 antibody-negative) were assessed at 8, 12, 20 and 28 weeks postpartum in the outpatients of a district general hospital. Thyroid antibody levels (antimicrosomal and antithyroglobulin) were monitored at monthly intervals, together with plasma T3, T4 and thyroid-stimulating hormone. The main outcome measures were Research Diagnostic Criteria for depression, the 17-item Hamilton Depression Rating Scale and the Edinburgh Postnatal Depression Scale, together with reaction time and digit span. Subjects with postnatal depression showed detectable cognitive impairment independent of thyroid antibody status and actual thyroid dysfunction.
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PMID:Cognitive function, thyroid status and postpartum depression. 762 5

Thyrotropin-releasing hormone (TRH) stimulation tests were performed in 27 women with autoimmune thyroiditis and concomitant DSM-III-R mood disorders. Increased thyrotropin (TTH) response to TRH stimulation (delta TTH > or = 25 microU/ml) was present only in 4 (14.8%) and blunted (delta TTH < 7 microU/ml) in 12 (44.4%) patients. The problem of hyperdiagnosis of hypothyroidism due to depression and methods of treatment of patients with autoimmune thyroiditis and concomitant affective disorders are discussed.
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PMID:[Affective pathology and the function of the hypothalamo-hypophyseal-thyroid system in women with autoimmune thyroiditis]. 774 Aug 77

Two thyroid axis findings are often reported in depressed patients: autoimmune thyroiditis and abnormal thyrotropin (thyroid stimulating hormone, TSH) responses to thyrotropin-releasing hormone (TRH). The TSH response to TRH can be exaggerated, suggesting subclinical hypothyroidism; it can alternatively be blunted, for reasons poorly understood. We selected 28 women who had been found to have major depression for TRH testing. Fifteen patients had autoimmune thyroiditis and 13 had diffuse nontoxic goiter. The endocrinological diagnoses were verified by fine-needle aspiration biopsy and cytological assessment. Patients with overt hypothyroidism and hyperthyroidism were excluded from the study. There were no differences between the two groups in total triiodthyronine and thyroxine plasma levels or severity of depression. In the autoimmune group, basal TSH and Dmax TSH tended to be higher (p < 0.1); peak TSH was significantly higher (p < 0.05), suggesting that the prevalence of subclinical hypothyroidism was also higher. Blunted TSH responses were found about as often in one group as the other.
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PMID:Thyrotropin response to TRH stimulation in depressed patients with autoimmune thyroiditis. 782 17


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