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Human thyroid stimulating hormone (hTSH) or thyrotropin is a glycoprotein synthesized by the basophilic cells (thyrotropes) of the anterior pituitary. hTSH is composed of two non-covalently linked subunits designated alpha and beta. Although the alpha subunit of hTSH is common to the luteinizing hormone (LH), follicle stimulating hormone (FSH) and human chorionic gonadotropin (hCG), the beta subunits of these glycoproteins are hormone specific and confer biological as well as immunological specificity. Both alpha and beta subunits are required for biological activity. hTSH stimulates the production and secretion of the metabolically active thyroid hormones, thyroxine (T4) and triiodothyronine+(T3), by interacting with a specific receptor on the thyroid cell surface.
T3 and T4 are responsible for regulating diverse biochemical processes throughout the body which are essential for normal development and metabolic and neural activity. The synthesis and secretion of hTSH is stimulated by thyrotropin releasing hormone (TRH), the hypothalamic tripeptide, in response to low levels of circulating thyroid hormones. Elevated levels of T3 and T4 suppress the production of hTSH via a classic negative feedback mechanism. Recent evidence also indicates that somatostatin and dopamine exert inhibitory control over hTSH release, suggesting that the hypothalamus may provide both inhibitory and stimulatory influence on pituitary hTSH production. Failure at any level of regulation of the hypothalamic-pituitary-thyroid axis will result in either underproduction (hypothyroidism) or overproduction (hyperthyroidism) of T4 and/or T3.
In cases of primary hypothyroidism, T3 and T4 levels are low and hTSH levels are significantly elevated. In the case of pituitary dysfunction, either due to intrinsic hypothalamic or pituitary disease; i.e., central hypothyroidism, normal or marginally elevated basal TSH levels are often seen despite significant reduction in T4 and/or T3 levels. These inappropriate TSH values are due to a reduction in TSH bioactivity which is frequently observed in such cases. Routine TRH stimulation is advised to confirm the diagnosis in such cases. Secondary hypothyroidism typically results in an impaired hTSH response to TRH, while in tertiary hypothyroidism the hTSH response to TRH may be normal, prolonged or exaggerated. Anomalies do occur, however, which limit the use of TRH response as the sole means of differentiating secondary from tertiary hypothyroidism. Although elevated hTSH levels are nearly always indicative of primary hypothyroidism, some rare clinical situations arise which are the result of a hTSH-secreting pituitary tumor (secondary hyperthyroidism). Such patients would display clinical signs of hyperthyroidism.
Primary hyperthyroidism (e.g. Grave's Disease, thyroid adenoma or nodular goiter) is associated with high levels of thyroid hormones and depressed or undetectable levels of hTSH. The TRH stimulation test has been used in diagnosis of hyperthyroidism. Hyperthyroid patients show a subnormal response to the TRH test. In addition, large doses of glucocorticoids, somatostatin, dopamine and replacement doses of thyroid hormones reduce or totally blunt the hTSH response to TRH.