Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001430 (adenoma)
 21,222 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The secretion and biological activity of thyroid stimulating hormone (TSH) were studied in 22 patients with a pituitary tumour (17 acromegalics and 5 patients with a chromophobe adenoma) and in 36 hypophysectomized patients (16 acromegalics and 20 with a chromophobe adenoma). Thyroid function was assessed by serum thyroxine (T4), serum triiodothyronine (T3), and thyroxine-binding globulin (TBG) concentration. Serum TSH was measured before and after injection of TSH releasing hormone (TRH), and in 19 hypophysectomized patients the T3 response after TRH was measured. In addition a TRH test was performed 1-2 weeks after surgery in 11 patients. The basal serum TSH did not differ from euthyroid control values in any of the groups and no late effect of hypophysectomy was observed. Subnormal peak TSH values were seen in 10 out of 37 euthyroid patients, whereas 9 out of 11 hypothyroid patients responded normally. Hypophysectomy caused an immediate but transient decrease in peak TSH in patients with a chromophobe adenoma only. The rise in serum T3 after TRH was significantly lower in hypophysectomized patients than in controls. An increase in TSH was followed by a T3 response in all patients except in 4 out of 8 euthyroid acromegalics. In patients operated on for a chromophobe adenoma the T3 response was correlated with serum T4, whereas this was not the case in acromegalics.
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PMID:Effect of thyrotrophin releasing hormone (TRH) in patients with pituitary disorders. 40 35

Little is known about the factors that cause exacerbations of autoimmune thyroid dysfunction. One possibility is an alteration in adrenocortical function, since glucocorticoids are known to alter both pituitary-thyroid and immunologic function. We encountered three patients in whom overt autoimmune thyroid disease developed after unilateral adrenalectomy for Cushing's syndrome due to an adrenocortical adenoma. We compared the postoperative changes in thyroid function in these patients with those in 21 other patients with Cushing's syndrome who underwent the same treatment. After unilateral adrenalectomy, one of the three patients had transient hyperthyroidism and a low thyroid uptake of 131I, indicative of silent thyroiditis. After the same surgical procedure, the second patient had hypothyroidism, where-as the third patient had transient hyperthyroidism at first, and hypothyroidism then gradually developed. All three patients had serum antithyroid antibodies, the titers of which increased after surgery. In the remaining 21 patients (only 2 of whom had antithyroid antibodies initially), the serum concentrations of thyroxine, triiodothyronine, and thyroxine-binding globulin and the secretion of thyroid-stimulating hormone increased after surgery from values that were low or near the lower limit of normal to values still well within the normal range. None of these patients had clinically evident thyroid disease or increased antithyroid-antibody titers. We conclude that reductions in the secretion of glucocorticoid may exacerbate subclinical autoimmune thyroid disease. Patients with Cushing's syndrome due to adrenocortical adenoma who have thyroid antibodies should be followed closely after treatment, because thyroid dysfunction may develop.
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PMID:Exacerbation of autoimmune thyroid dysfunction after unilateral adrenalectomy in patients with Cushing's syndrome due to an adrenocortical adenoma. 234 40

Plasma concentrations of T4, FT4, T3, rT3 and TBG, as well as of TSH before and after stimulation with TRH were studied in 25 patients, who had been treated with amiodarone for up to nine years. At the beginning of therapy, all the parameters mentioned above were found to be in the normal range in all patients. After two months of therapy, T4 had increased from 100 nmol/l +/- 24 nmol/l to 155 nmol/l +/- 32 nmol/l (p less than 0.01), and FT4 from 22 pmol/l +/- 10.5 pmol/l to 32 pmol/l +/- 8 pmol/l (p less than 0.01). T3 had decreased to the lower normal range (n.s.). TBG showed no significant changes. The TRH-tests had been normal in the beginning, but they remained positive in only 20% of the cases. At the end of the study, rT3 exceeded the normal range in all 25 patients. Two patients developed definite hyperthyroidism with elevations of T3 up to 4.7 nmol/l and 7.5 nmol/l, respectively. In one of them, we decided to discontinue amiodarone. Testing of thyroid function under antithyroid drug therapy revealed a hyperfunctioning autonomous adenoma, which was successfully eliminated by radioactive iodine therapy. In the other patient, it was not possible to withdraw amiodarone, so we initiated long-term treatment with antithyroid drugs. Our data support the assumption that amiodarone causes an impairment of the peripheral conversion of T4 to T3. As a result, one finds elevated serum concentrations of T4, which, in combination with the mainly negative TRH-test, must not be interpreted as proof of a hyperthyroid metabolic state being present. Hyperthyroidism is confirmed only if serum concentrations of T3 are also elevated.
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PMID:[The effect of amiodarone on thyroid gland function]. 647 80

We found transient hyperthyroidism in the course of hydrocortisone withdrawal in two patients who had undergone unilateral adrenalectomy to resect cortisol-hypersecreting adenoma. A 38-yr-old woman showed clinical thyrotoxicosis 3 months after the operation. Serum T4, T3 and TBG levels were 11.9 micrograms/dl, 310 ng/dl and 16.5 micrograms/ml, respectively. She was given methimazole (MMI) 15 mg/day for 4 weeks. After the cessation of MMI treatment, she eventually recovered to the euthyroid state. The other patient, a 34-yr-old man showed very mild clinical symptoms of hyperthyroidism 2 months after the operation. Serum T4, T3 and TBG levels were 10.4 micrograms/dl, 240 ng/dl and 14.5 micrograms/ml, respectively. In this case, no antithyroid drug was given. Two to three months after the onset of hyperthyroidism, he returned to the euthyroid state spontaneously. We carefully eliminated the possibility of factitious thyrotoxicosis in both cases. They had neither neck pain nor fever. Both had low radioactive iodine uptake by the thyroid. Therefore, we diagnosed them as painless thyroiditis induced after the resection of hypersecreting adrenal adenoma.
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PMID:Transient thyrotoxicosis after unilateral adrenalectomy in two patients with Cushing's syndrome. 651 31

Few data are available on serum free thyroid hormone concentration in patients with T3-toxicosis. In this study total and free T4 and T3 and TBG were evaluated in 35 subjects with T3-toxicosis, including 12 with untreated Graves' disease, 5 Graves' patients on methimazole treatment, 13 with autonomous adenoma, 3 with multinodular goiter, and 2 with subacute thyroiditis. T4, T3, free T4 (FT4), free T3 (FT3) as well as calculated T4/TBG and T3/TBG ratios were significantly higher in patients than in 37 healthy controls. Serum FT4 levels above the normal range were found in 19 subjects with T3-toxicosis (9 with untreated and one with methimazole-treated Graves' disease, 6 with autonomous adenoma, 1 with multinodular goiter and 2 with subacute thyroiditis). These data, together with the few previous reports, indicate that high FT4 levels are present in about half of the patients with so called T3-toxicosis, and that this occurs more frequently in diffuse than nodular goiter. It is suggested that the term T3-toxicosis be used only for those subjects with normal total and free T4.
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PMID:Serum free thyroid hormones in T3-toxicosis: a study of 35 patients. 668 30