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)

Suppression of TSH and thyroid radioiodine uptake by doses of either T4 or T3 were compared in 33 patients in whom Graves' thyrotoxicosis had been treated with thioamide drugs and the medication was discontinued for at least 4 months. Thyroidal radiodine uptake was suppressed in 19 patients and was not suppressed in the remaining 14 patients. Basal TSH levels before suppression were 2.07 microU/ml in the former, significantly exceeding those of the latter (0.91 microU/ml). A TSH level of at least 1.2 microU/ml before suppression is a good predictor of positive thyroid radioiodine suppression with a predictive value of 76%. A level lower than 0.7 microU/ml before suppression is a good predictor of negative thyroid radioiodine uptake suppression with a predictive value of 89%. The determination of TSH levels before the thyroid suppression test was helpful in predicting the result, but there were limitations. In the thyroid suppression test positive group, circulating T4 was depressed by doses of T3. In them, the magnitude of T4 depression correlated with the levels of thyroid radioiodine uptake before suppression. The levels of TSH correlated neither to changes in T4 nor to those in thyroid radioiodine uptake. This indicates that the thyroid glands which show high radioiodine uptake are sensitive to TSH and are also sensitive to suppression. The elevated sensitivity to TSH probably warrants the disappearance of abnormal thyroid stimulation more precisely.
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PMID:Highly sensitive immunoradiometric assay for TSH and thyroid radioiodine uptake as predictors of thyroid suppression test. 367 55

Studies of in vitro immunoreactivity to propylthiouracil (PTU), methimazole (MMI), and carbimazole (CARB), as assessed by peripheral blood lymphocyte transformation and 2 antibody tests, were carried out in 12 patients with Graves' hyperthyroidism who had developed agranulocytosis during treatment with PTU (11 patients) or CARB (1 patient) from 1 week to 10 yr earlier. Significant lymphocyte transformation responses to antithyroid drugs (stimulation indices greater than mean +/- 2 SD for normal subjects) were found in 5 of 6 patients tested, in 1 patient to PTU only, in 3 patients to MMI only, and in 1 patient to both PTU and MMI, but in none of 10 patients currently being treated with PTU who did not develop agranulocytosis. Circulating antibodies causing neutrophil agglutination in the presence of antithyroid drugs were demonstrated, using the indirect Coombs test, in 5 of 7 patients tested, in 2 patients to PTU only, in 3 patients to CARB only and in 1 patient (the only one tested with MMI) to PTU and MMI. Lymphocyte transformation and antibody tests to PTU were both carried out in 6 patients. Of these, both tests were positive in one patient, both negative in 3 patients, and 1 negative and 1 positive in 2 patients. In the 1 patient in whom both tests were carried out with CARB (patient 3), tests were negative, whereas in the 1 patient in whom both tests were carried out with MMI (patient 3), 1 test was positive, whereas the other was negative. Thus, in patients in whom both tests were carried out using the same drug, correlation between lymphocyte transformation responses and the detection of neutrophil antibodies was found in 5 of 6 cases. Antibodies reactive with neutrophils were also detected in 2 of the 5 patients tested using an enzyme-linked immunosorbent assay. In this test antibodies to PTU or MMI were not demonstrated. Possible mechanisms for the neutrophil depression in relation to these findings are discussed. It is concluded that patients with Graves' disease may be prone to develop this complication of antithyroid drug therapy because of underlying immunological abnormalities.
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PMID:In vitro immunoreactivity to propylthiouracil, methimazole, and carbimazole in patients with Graves' disease: a possible cause of antithyroid drug-induced agranulocytosis. 620 Apr 92

In some children, psychological events have appeared to be important in the triggering of Graves' disease. This report examines the case histories of three children in whom the appearance of symptomatology of Graves' disease was associated with depression following the death of a loved one. An analysis of neuroendocrine and immunologie pathways suggests that depression, set off by bereavement, causes low levels of norepinephrine in the brain. The latter in turn may mediate an increase in ACTH and cortisol, leading to reductions in immune surveillance and resultant production of thyroid-stimulating immunoglobulins, hence the development of Graves' disease.
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PMID:Activation of latent Graves' disease in children. Review of possible psychosomatic mechanisms. 624 27

In an attempt to study the mode of normalization of thyroid function in patients with Graves' disease, a study was made on 140 patients with Graves' disease who were eumetabolic after appropriate therapy with antithyroid drugs for more than 9 months. T3 administration failed to suppress thyroidal radioiodine uptake and serum T4 in patients with TRH-unresponsive TSH secretion. In addition, exogenous TSH failed to elevate serum levels of T4 and T3. In patients with TRH-responsive pituitaries, T3 administration uniformly made serum TSH undetectable but produced various effects (unsuppressible, partially suppressible, and suppressible) on radioiodine uptake and serum T4. The magnitude of suppression of radioiodine uptake paralleled that of serum T4. In patients with unsuppressible or partially suppressible thyroids, exogenous and endogenous TSH were less effective in elevating serum T4 and T3. In patients with suppressible thyroids, T3 administration depressed radioiodine uptake and serum T4; the magnitudes of depression were comparable to those found in normal subjects. Exogenous and endogenous TSH elevated serum T4 and T3 in patients with suppressible thyroids. Here again, the magnitudes of elevation were comparable to those found in the normal subjects. The serum T3 to T4 ratio was high before treatment, but decreased significantly during antithyroid drug therapy. The magnitude of decrease was roughly proportional to the degree of T3 suppressibility.
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PMID:Pituitary-thyroid feedback regulation in patients with Graves' disease during antithyroid drug therapy. 679 61

There are few reported convincing cases of hyperthyroid depressed patients receiving electroconvulsive therapy (ECT). We describe a depressed 66-year-old woman with catatonic depression diagnosed with new-onset hyperthyroidism due to Grave's disease. After commencing propylthiouracil, her Grave's disease was partially treated, but her depression was no better. She subsequently received a course of seven ECT with resolution of her depression and no adverse sequelae.
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PMID:ECT administration to a hyperthyroid patient. 755 52

In an attempt to study "manic-depressive" affairs associated with endocrine and mental disorders, our clinical data are analyzed before and after appropriate treatment in Cushing's disease, Cushing's syndrome, hyperthyroid Graves' disease and primary hypothyroidism. Although our data do not provide definite findings on manic-depressive affairs associated with Cushing's disease and syndrome, review data by others indicated a high incidence of depression under untreated condition and its disappearance after appropriate treatment. In contrast, patients with adrenocortical insufficiency did have a depression but this was cleared after supplemental therapy. In hyperthyroid Graves' disease, a number of emotional and mental instability and irritability were noticed before the treatment, but these abnormalities all disappeared after appropriate treatment for 3-6 months. In contrast, patients with primary hypothyroidism did show lethargy and apathy, and these abnormalities disappeared after appropriate treatment. From the data accumulated, it is concluded that adrenal steroid and thyroid hormone do affect the functions of nervous system and, as a result, cause a number of clinical symptoms. The exact biochemical processes underlying these abnormalities are not known and remains for further investigations.
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PMID:[Manic-depressive symptom associated with endocrine and metabolic disorders]. 800 7

Depression in a common, life-threatening complication of Cushing's syndrome and may occur in several other endocrine disorders. It is not clear, however, whether distinct features pertain to hypercortisolism. We studied depression in Cushing's syndrome differentiating pituitary-dependent and pituitary-independent forms, its incidence compared to Graves' disease, and its appearance in the prodromal phase of both conditions. To 66 consecutive patients with Cushing's syndrome and 70 with Graves' disease, after treatment, a semistructured interview for depressive symptoms based on Paykel's clinical interview for depression was administered. In Cushing's syndrome, the response of depression to normalization of urinary cortisol levels was evaluated by Kellner's global rating method. There was a significant difference in the occurrence of depression (p < 0.001) between Cushing's syndrome (62%) and Graves' disease (23%). Depression appeared in the prodromal phase in 27% of patients with Cushing's syndrome and in 14% of those with Graves' disease, but the difference was not significant. In Cushing's syndrome, there were no significant differences in depression between patients with pituitary-dependent (n = 41) and pituitary-independent (n = 20) forms, or in their response to treatment. About 70% of patients fully recovered from their depression, whereas there was no substantial change in the others and even worsening in 2. Our findings in Cushing's syndrome and Graves' disease are in agreement with previous investigations using specific diagnostic criteria for depression. We found a tendency for this symptom to manifest in the prodromal phase of both illnesses. An endocrine etiology should be, therefore, considered in depressed patients not responding to standard psychiatric treatment.
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PMID:Course of depression in Cushing's syndrome: response to treatment and comparison with Graves' disease. 831 4

The following paper deals with the current research in hyperthyroidism, with special accent to Graves' disease. Besides severe psychological trauma a breakdown of neurotic defense mechanism on the ground of a special personality structure was thought to be the trigger of the disease. The metabolic changes became the main point of interest. The influence of thyrostatic, surgical and radioactive therapies on psychological symptoms, was investigated. Thereby, the previously anticipated emotional factors became less significant in the aetiology of the disease. A recent study (Paschke 1990) suggests that patient with hyperthyroidism have, even in an euthyrotic state, an increased vulnerability to anxiety provoking situations. At this point it is not clear, due to the retrospective nature of the study, whether the vulnerability exists prior to the unset of the disease or is a result of the metabolic disorder. Both thyroxin and TRH are being successfully used in the treatment of major depression. TRH acts as a neurotransmitter in the autonomic nervous system and can be demonstrated in the peripheral lymphocytes. However, the exact mechanisms of action of thyroxin and TRH are still unknown. Graves' disease is an autoimmune disease, that can be caused by specific HLA antigens. Thereby, a changed subpopulation of lymphocytes can be demonstrated, as well as there disturbed functions. A correlation between high scores for anxiety and depression on one hand and the occurrence of an abnormal T4/T8 ratio on the other hand, have been reported in a small number of cases (Paschke 1990). The psychological symptoms in hyperthyroidism are similar to the symptomatology of neurotic anxiety and the anxious depressive syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Psychosomatic aspects of hyperthyroidism with special reference to Basedow's disease. An overview]. 837 18

Postpartum thyroid dysfunction (PTD) occurs in approximately 5% to 10% of all women within 1 year following delivery and is usually due to intrinsic thyroid disease rather than hypothalamic or pituitary lesions. The most common etiology of PTD, which may resemble postpartum depression, is autoimmune thyroid disease (chronic or Hashimoto's thyroiditis). Women with Graves' disease who experience symptom exacerbation in the postpartum period account for a small percentage of cases. Clues to PTD include nonspecific symptoms such as tiredness, fatigue, depression, palpitations, and irritability. On physical examination, tachycardia may be noted. Goiters are detected in the majority of cases. The disease course varies; most patients experience a phase of hypothyroidism that takes 2 to 6 months to resolve, but some develop permanent hypothyroidism within 5 years of the diagnosis.
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PMID:Evaluating and Managing Postpartum Thyroid Dysfunction. 974 99

Natural killer (NK) cell activity of peripheral blood lymphocytes (PBL) against k562 human tumor cell targets was studied in patients with Graves' disease and Hashimoto's thyroiditis. NK activity was measured in a standard 4-hour 51chromium (Cr) release assay. Cytotoxicity was expressed as lytic units (LU)/10(6) PBL. Significantly decreased NK cell activity was demonstrated in both groups of patients, with mean (+/- SE) lytic units of 10.3 (+/- 9.1) and 13.3 (+/- 10.3) for patients with Graves' disease and Hashimoto's thyroiditis, respectively, compared with 36.0 (+/- 26.3) for age- and sex-matched normal subjects. When patients with Graves' disease were analyzed according to their thyroid status; NK activity was significantly depressed in (1) hyperthyroid patients before treatment; (2) hyperthyroid patients receiving antithyroid therapy; and (3) euthyroid patients receiving antithyroid therapy, compared with normal subjects. Graves' disease patients who were hypothyroid after radioactive iodine therapy or thyroidectomy had normal NK activity. No significant differences between hyperthyroid and euthyroid patients or between hypothyroid patients and normal subjects were demonstrated. NK activity in patients with Graves' disease did not correlate with serum levels of thyroxine, the presence or severity of ophthalmopathy, or titers of serum thyroid antibodies. In patients with Hashimoto's thyroiditis there was no correlation between NK activity and goiter size, titers of antithyroid antibodies, or thyroid status. These findings suggest that depression of NK activity in both disorders is secondary to abnormalities of thyroid hormone secretion, although an effect of the underlying autoimmune reactions has not been excluded.
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PMID:Natural killer cell activity in patients with Graves' disease and Hashimoto's thyroiditis. 984 16


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