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TSH levels are determined by a classic negative feedback system in which high levels of T3 and T4 suppress the production of TSH, and low levels of T3 and T4 increase the production of TSH. TSH levels are thus often used by doctors as a screening test, where the first approach is to determine whether TSH is elevated, suppressed, or normal. [25]
An increase in TSH above the normal range indicates under-replacement or poor compliance with therapy. A significant reduction in TSH suggests over-treatment. In both cases, a change in dose may be required. A low or low-normal TSH value may also signal pituitary disease in the absence of replacement. [citation needed]
Low-T3 syndrome and high-T3 syndrome: Consequences of step-up hypodeiodination, e.g. in critical illness as an example for type 1 allostasis, [20] or hyperdeiodination, as in type 2 allostasis, including posttraumatic stress disorder. [12] Resistance to thyroid hormone: Feedback loop interrupted on the level of pituitary thyroid hormone receptors.
Thyroid-stimulating hormone (TSH) released from the anterior pituitary (also known as the adenohypophysis) binds the TSH receptor (a G s protein-coupled receptor) on the basolateral membrane of the cell and stimulates the endocytosis of the colloid. The endocytosed vesicles fuse with the lysosomes of the follicular cell.
If the TSH level is normal or low and serum free T 4 levels are low, this is suggestive of central hypothyroidism (not enough TSH or TRH secretion by the pituitary gland or hypothalamus). There may be other features of hypopituitarism , such as menstrual cycle abnormalities and adrenal insufficiency .
Therefore, when TRH is given exogenously, TSH levels increase. If the increase in serum TSH level following TRH administration is absent or very slight, then the cause of the hypothyroidism is in the anterior pituitary gland, i.e. the pituitary is not secreting TSH. Therefore, even when TRH is given exogenously, TSH levels do not rise as the ...