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|Thyroid-stimulating hormone, alpha|
|Alt. symbols||HCG, GPHa, GPHA1|
|Locus||Chr. 6 q14-q21|
|Thyroid-stimulating hormone, beta|
|Locus||Chr. 1 p13|
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, TSH, or hTSH for human TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T4), and then triiodothyronine (T3) which stimulates the metabolism of almost every tissue in the body. It is a glycoprotein hormone synthesized and secreted by thyrotrope cells in the anterior pituitary gland, which regulates the endocrine function of the thyroid. In 1916, Bennett M. Allen and Philip E. Smith found that the pituitary contained a thyrotropic substance.
TSH (with a half life of about an hour) stimulates the thyroid gland to secrete the hormone thyroxine (T4), which has only a slight effect on metabolism. T4 is converted to triiodothyronine (T3), which is the active hormone that stimulates metabolism. About 80% of this conversion is in the liver and other organs, and 20% in the thyroid itself.
TSH is secreted throughout life but particularly reaches high levels during the periods of rapid growth and development.
Somatostatin is also produced by the hypothalamus, and has an opposite effect on the pituitary production of TSH, decreasing or inhibiting its release.
The concentration of thyroid hormones (T3 and T4) in the blood regulates the pituitary release of TSH; when T3 and T4 concentrations are low, the production of TSH is increased, and, conversely, when T3 and T4 concentrations are high, TSH production is decreased. This is an example of a negative feedback loop. Any inappropriateness of measured values, for instance a low-normal TSH together with a low-normal T4 may signal tertiary (central) disease and a TSH to TRH pathology. Elevated reverse T3 (RT3) together with low-normal TSH and low-normal T3, T4 values, which is regarded as indicative for euthyroid sick syndrome, may also have to be investigated for chronic subacute thyroiditis (SAT) with output of subpotent hormones. Absence of antibodies in patients with diagnoses of an autoimmune thyroid in their past would always be suspicious for development to SAT even in the presence of a normal TSH because there is no known recovery from autoimmunity.
|Source of pathology||TSH level||Thyroid hormone level||Disease causing conditions|
|Hypothalamus/pituitary||High||High||Benign tumor of the pituitary (adenoma) or thyroid hormone resistance|
|Hypothalamus/pituitary||Low||Low||Secondary hypothyroidism or "central" hypothyroidism|
|Hyperthyroidism||Low||High||Primary hyperthyroidism i.e. Graves' disease|
|Hypothyroidism||High||Low||Congenital hypothyroidism (cretinism), Primary hypothyroidism i.e. Hashimoto's thyroiditis|
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