![]() The National Academy of Clinical Biochemistry (NACB) stated that it expected the reference range for adults to be reduced to 0.4–2.5 µIU/mL, because research had shown that adults with an initially measured TSH level of over 2.0 µIU/mL had "an increased odds ratio of developing hypothyroidism over the 20 years, especially if thyroid antibodies were elevated". ![]() In the UK, guidelines issued by the Association for Clinical Biochemistry suggest a reference range of 0.4–4.0 µIU/mL (or mIU/L). Reference ranges for TSH may vary slightly, depending on the method of analysis, and do not necessarily equate to cut-offs for diagnosing thyroid dysfunction. Applications Diagnostics įurther information: Thyroid function tests This is also the mechanism of trophoblastic tumors increasing the production of thyroid hormones. In pregnancy, prolonged high concentrations of hCG can produce a transient condition termed gestational hyperthyroidism. In addition, hCG shows some cross-reactivity to the TSH receptor and therefore can stimulate production of thyroid hormones. Stimulating antibodies to the TSH receptor mimic TSH and cause Graves' disease. ![]() (6) Secretion of thyroxine (T 4) and triiodothyronine (T 3) across the basolateral membrane of follicular cells to enter the circulation. (5) Stimulation of proteolysis of iodinated thyroglobulin to form free thyroxine (T 4) and triiodothyronine (T 3). (4) Increased endocytocis of the iodinated thyroglobulin protein across the apical membrane back into the follicular cell. This leads to the formation of thyroxine (T 4) and triiodothyronine (T 3) that remain attached to the thyroglobulin protein. (3) Stimulating the conjugation of iodinated tyrosine residues. (2) Stimulating iodination of thyroglobulin in the follicular lumen, a precursor protein of thyroid hormone. This occurs through stimulation of six steps in thyroid hormone synthesis: (1) Up-regulating the activity of the sodium-iodide symporter (NIS) on the basolateral membrane of thyroid follicular cells, thereby increasing intracellular concentrations of iodine (iodine trapping). Stimulation of the receptor increases T 3 and T 4 production and secretion. The TSH receptor is found mainly on thyroid follicular cells. The β chain has a 118-amino acid sequence. The β ( beta) subunit ( TSHB) is unique to TSH, and therefore determines its receptor specificity.The α chain has a 92-amino acid sequence. The α subunit is thought to be the effector region responsible for stimulation of adenylate cyclase (involved the generation of cAMP). The α ( alpha) subunit (i.e., chorionic gonadotropin alpha) is nearly identical to that of human chorionic gonadotropin (hCG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH).TSH is a glycoprotein and consists of two subunits, the alpha and the beta subunit. 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.įor clinical interpretation of laboratory results it is important to acknowledge that TSH is released in a pulsatile manner resulting in both circadian and ultradian rhythms of its serum concentrations. Elevated reverse T 3 (RT 3) together with low-normal TSH and low-normal T 3, T 4 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. Any inappropriateness of measured values, for instance a low-normal TSH together with a low-normal T 4 may signal tertiary (central) disease and a TSH to TRH pathology. This is an example of a negative feedback loop. The concentration of thyroid hormones (T 3 and T 4) in the blood regulates the pituitary release of TSH when T 3 and T 4 concentrations are low, the production of TSH is increased, and, conversely, when T 3 and T 4 concentrations are high, TSH production is decreased. Somatostatin is also produced by the hypothalamus, and has an opposite effect on the pituitary production of TSH, decreasing or inhibiting its release. ![]() TRH stimulates the anterior pituitary gland to produce TSH. The hypothalamus, in the base of the brain, produces thyrotropin-releasing hormone (TRH). TSH is secreted throughout life but particularly reaches high levels during the periods of rapid growth and development, as well as in response to stress. About 80% of this conversion is in the liver and other organs, and 20% in the thyroid itself. T 4 is converted to triiodothyronine (T 3), which is the active hormone that stimulates metabolism. TSH (with a half-life of about an hour) stimulates the thyroid gland to secrete the hormone thyroxine (T 4), which has only a slight effect on metabolism. ![]() See also: Hypothalamic–pituitary–thyroid axis ![]()
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