TSH-induced Hyperthyroidism Research Articles

Pituitary adenoma with gigantism and TSH-induced hyperthyroidism: a case report

Searchable abstracts of presentations at key conferences in endocrinology ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

TSH-induced hyperthyroidism caused by a pituitary tumor

A 45-year-old man presented with frontal headache and visual disturbances to our clinic. For the previous 5 years, he had been receiving treatment for long-lasting mild hyperthyroidism with antithyroid therapy, but therapy had not been carefully followed. During the last 2 years he had also complained of erectile dysfunction and loss of libido. On physical examination, he had a small goiter, normal skin, no Graves' ophthalmopathy, normal BMI, and reduced testis volume and pubic hair. Serum levels of free T3 and T4, serum prolactin, testosterone, serum gonadotropins, insulin-like growth factor 1, adrenocorticotropic hormone, and cortisol were measured. MRI scan, TSH-releasing hormone test, and T3 suppression test were carried out. Levels of pituitary glycoprotein hormone alpha-subunit and sex-hormone-binding protein were also measured. Hyperthyroidism caused by a mixed pituitary adenoma that secretes prolactin and TSH. Trans-sphenoidal resection of the pituitary tumor. After surgery, T3 suppression test failed to completely suppress TSH secretion, which suggested a persistence of residual adenomatous cells. Hyperthyroidism and hypogonadism recurred after 5 years, therefore, treatment with lanreotide was initiated, and resulted in complete resolution of signs and symptoms of the disease.

Hyperthyroidism due to a Pituitary Adenoma Composed of Two Different Cell Types, One Secretingα-Subunit Alone and Another Cosecretingα-Subunit and Thyrotropin*

A 37-yr-old female presented with clinical signs and symptoms of mild hyperthyroidism, high serum levels of free T4 (24.2 pmol/L), free T3 (11.7 pmol/L), and sex hormone-binding globulin (157 nmol/L) as well as measurable (by immunofluorometric assay) serum TSH concentrations (1.9 mU/L) in the absence of any known methodological interference. The above finding indicated the presence of hyperthyroidism due to inappropriate secretion of TSH, whose neoplastic origin was documented by computed tomographic scan showing a 1-cm pituitary adenoma. The diagnosis was confirmed by elevated alpha-subunit levels (9.2 micrograms/L) and alpha-subunit/TSH molar ratio (25.2) as well as absent TSH suppression after T3 administration. TRH injection (200 microgram, iv) caused impaired TSH (from 3.0 to 4.8 mU/L) and unexpectedly exaggerated alpha-subunit (from 8.8 to 18.2 micrograms/L) responses. Such a discrepancy was also observed after other dynamic tests. Double gold particle immunostaining of the adenomatous tissue removed at surgery showed that all of the cells contained secretory granules positive for alpha-subunit, while very few cells were positive for TSH beta and alpha-subunit. In conclusion, the present study demonstrates the existence of TSH-induced hyperthyroidism due to a pituitary adenoma composed of two different cell types: one secreting alpha-subunit alone and another cosecreting alpha-subunit and TSH.

10 Years of Successful Treatment with Dextrothyroxine in a Girl with TSH-Induced Hyperthyroidism

14 years ago, a 5.7-year-old healthy girl was treated with desiccated thyroid for a goiter and elevated TSH levels. The goiter disappeared and TSH levels were normalized. However, hyperthyroidism appeared. Without therapy, the goiter reappeared and hyperthyroidism aggravated. Based on hormone values, TSH-induced hyperthyroidism was diagnosed. After exclusion of neoplastic TSH secretion, treatment with dextrothyroxine (DT4) was initiated at age of 10 years and continued during the last 10 years (except for short periods). The girl became euthyroid, has no goiter and normal TSH values. Since thyrotrophs and peripheral tissues are probably normally sensitive to T4, we postulate that her hypothalamopituitary-thyroid control is operating on a higher set point level for T4.

Clinical hyperthyroidism due to non-neoplastic inappropriate thyrotrophin secretion

We report a case of hyperthyroidism due to inappropriate thyrotrophin (TSH) secretion in a patient with selective pituitary resistance to thyroid hormone action. Symptoms of hyperthyroidism in patients with this disorder are usually mild, implying some peripheral tissue resistance to the metabolic effects of thyroid hormone. Our patient had unusually severe symptoms, including marked weight loss and cardiac arrythmias which required carbimazole and beta-blocker therapy for control. Somatostatin was ineffective in suppressing TSH secretion. The introduction of sensitive thyrotrophin assays should facilitate the accurate diagnosis of TSH-induced hyperthyroidism and avoid inappropriate treatment.

Central Hypothyroidism and Hyperthyroidism

Thyroid function is maintained by tonic secretion of TSH by the pituitary. TSH secretion, in turn, is dependent on hypothalamic TRH production. Therefore, diseases of the hypothalamus and pituitary are frequently associated with TSH deficiency, producing central hypothyroidism. All patients with hypothalamic or pituitary disease should have thyroid function tests including a serum TSH by radioimmunoassay (RIA). In central hypothyroidism the TSH RIA is inappropriately low in relationship to the degree of hypothyroxinemia but is not always undetectable. In fact, because of the production of biologically inactive TSH, the TSH RIA may be in the high range of normal. Therapy of central hypothyroidism includes the management of associated pituitary hormone deficiencies, particularly secondary adrenal failure, and neurologic defects. A rare cause of hyperthyroidism is excessive TSH secretion. This may be due to a TSH-secreting pituitary tumor or to a functional disturbance in TSH secretion. TSH-secreting pituitary tumors are often large and locally invasive. Selective pituitary resistance to thyroid hormone is the most common cause of functional TSH-induced hyperthyroidism. It is important to rule out generalized thyroid hormone resistance before use of antithyroid drugs or thyroid surgery in patients suspected of this disorder. This is because antithyroid treatment is contraindicated in generalized thyroid hormone resistance.

High plasma thyrotrophin levels in two patients with pituitary tumour.

ABSTRACT Out of 62 patients with pituitary tumours two (B. M.: vascular tumour and D. G.: chromophobe adenoma) showed symptoms and signs of hyperthyroidism and high plasma thyrotrophin (HTSH) values (mean values 24.0 and 8.4 μU/ml respectively). A parallelism was found between the Human Thyroid Stimulating Hormone Research Standard A (HTSH RSA) and the plasma dilution curves suggesting identity between immunoreactive material and authentic HTSH. The biological TSH activity was determined by McKenzie bioassay. Methimazole administration did not induce any significant modification in case B. M. while in case D. G. it caused a further increase in plasma HTSH. The triiodothyronine suppression test carried out in patient B. M. failed to produce a full inhibition, suggesting an autonomous function of the TSH secreting system. Lysine-vasopressin was ineffective in promoting HTSH increases in both cases, while insulin induced hypoglycaemia provoked in case B. M. a prompt fall in plasma HTSH levels, followed by an increase over the base line. The data obtained in case B. M. are compatible with a TSH-induced hyperthyroidism, while those found in patient D. G., though suggestive, are not completely consistent with this interpretation.