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Jostel's TSH index (TSHI or JTI), also referred to as Jostel's thyrotropin index or Thyroid Function index (TFI), is a method for estimating the thyrotropic (i.e. thyroid stimulating) function of the anterior pituitary lobe in a quantitative way. [1] [2] The equation has been derived from the logarithmic standard model of thyroid homeostasis.
Thyroid's secretory capacity (G T, also referred to as thyroid's incretory capacity, maximum thyroid hormone output, T4 output or, if calculated from serum levels of thyrotropin and thyroxine, as SPINA-GT [a]) is the maximum stimulated amount of thyroxine that the thyroid can produce in a given time-unit (e.g. one second).
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.
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 [following] 20 years, especially if ...
from quantiles of FT4 and TSH concentration (as determined based on cumulative distribution functions). [1] Per definition the TFQI has a mean of 0 and a standard deviation of 0.37 in a reference population. [1] This explains the reference range of –0.74 to + 0.74.
The Thyrotroph Thyroid Hormone Sensitivity Index (abbreviated TTSI, also referred to as Thyrotroph T4 Resistance Index or TT4RI) is a calculated structure parameter of thyroid homeostasis. It was originally developed to deliver a method for fast screening for resistance to thyroid hormone .
The TSH, in turn, stimulates the thyroid to produce thyroid hormone until levels in the blood return to normal. Thyroid hormone exerts negative feedback control over the hypothalamus as well as anterior pituitary, thus controlling the release of both TRH from hypothalamus and TSH from anterior pituitary gland.
In primary hyperthyroidism TSH are low and TRH administration induces little or no change in TSH levels • In hypothyroidism due to end organ failure, administration of TRH produces a prompt increase in TSH • In hypothyroidism due to pituitary disease (secondary hypothyroidism) administration of TRH does not produce an increase in TSH