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Thyroid function tests (TFTs) is a collective term for blood tests used to check the function of the thyroid. [1] TFTs may be requested if a patient is thought to suffer from hyperthyroidism (overactive thyroid) or hypothyroidism (underactive thyroid), or to monitor the effectiveness of either thyroid-suppression or hormone replacement therapy.
Thyroid-stimulating hormone (also known as thyrotropin, thyrotropic hormone, or abbreviated TSH) is a pituitary hormone that stimulates the thyroid gland to produce thyroxine (T 4), and then triiodothyronine (T 3) which stimulates the metabolism of almost every tissue in the body. [1]
Recent research suggested the existence of an additional feedforward motif linking TSH release to deiodinase activity in humans. [6] [7] [8] The existence of this TSH-T3 shunt could explain why deiodinase activity is higher in hypothyroid patients and why a minor fraction of affected individuals may benefit from substitution therapy with T3. [9]
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 pituitary is diseased. [citation needed]
TSH release in turn is stimulated by thyrotropin releasing hormone (TRH), released in a pulsatile manner from the hypothalamus. [39] The thyroid hormones provide negative feedback to the thyrotropes TSH and TRH: when the thyroid hormones are high, TSH production is suppressed. This negative feedback also occurs when levels of TSH are high ...
The first laboratory test to help assess thyroid status was the serum protein-bound iodine, which came into use around the 1950s. In 1971, the thyroid stimulating hormone (TSH) radioimmunoassay was developed, which was the most specific marker for assessing thyroid status in patients. [82]
Thyroid hormones (T 4 and T 3) are produced by the follicular cells of the thyroid gland and are regulated by TSH made by the thyrotropes of the anterior pituitary gland. The effects of T 4 in vivo are mediated via T 3 (T 4 is converted to T 3 in target tissues). T 3 is three to five times more active than T 4.
Stress suppresses TSH, [5] and alterations in thyroid hormone levels may arise in psychiatric illness. In major depressive disorder, an NTIS-like phenotype may be observed, with reduced T3 and increased rT3. T4 may be elevated, and TSH is usually normal, although TSH's normal circadian rhythm may be disrupted. [2]