Regulação da síntese e secreção de tireotrofina

Abstract

The set point of thyrotropin (TSH) secretion is determined by the balance of a positive regulation of thyrotropin releasing hormone (TRH) and the strong negative regulation exerted by thyroid hormones. In addition, there are other regulators superimposed on this main axis such as somatostatin and dopamine, which act as inhibitors of TSH secretion, and central alpha-adrenergic pathways that are predominantly stimulatory and involved in the cold-induced thyroid activation. Nutritional status and leptin also regulate TSH by stimulating TRH neurons through direct and indirect mechanisms. Stress is also involved in lowering TRH/TSH secretion possibly through glucocorticoids, cytokines and opioids. Recently, a new regulatory pathway has been proposed, via peptides produced in pituitary, acting in an autocrine/paracrine manner. Among those, more consistent data are available on neuromedin B, gastrin-releasing peptide and pituitary leptin, which act as local inhibitors of TSH release. Neonatal programming of TSH secretion set point is also discussed.

Thyroid abnormalities in term infants with fungal sepsis

“…This hormone stimulates the increase in serum T3, which is essential for activation of type 1 deiodinase (D1) enzyme between 4 and 6 hours after birth, and very low levels of reverse T3. [19][20][21][22][23][24][25][26][27][28] Currently, four stages of NTIS are recognized in adults and children, known as low T3 syndrome, low T3-T4 syndrome, high T4 syndrome, and mixed syndromes. [4][5][6][7][8][9][10][20][21][22][23][24][25][26][27][28] Low T3 syndrome This is characterized by low serum levels of T3, normal or slightly increased TSH, and normal free T4 and T4.…”

“…Evidence indicates that low T3 syndrome may be an adaptive response to stress, without association with worse prognoses or increased mortality. [22][23][24][25][26][27][28] For Papanicolaou, low T3 syndrome corresponds to the first stage of non-thyroidal illness syndrome. 6 Low T3-T4 syndrome This is characterized by the presence of low T4 and T3, with low TSH being frequent, alongside normal or high reverse T3.…”

“…It is currently believed that a mechanism occurs in this type of NTIS related to the effects of cytokines in the hypothalamic-pituitary axis, associated with reduced peripheral T4 action. [4][5][6][7][8][9][10][11][12][19][20][21][22][23][24][25][26][27][28] The response of TSH to thyrotropin-releasing hormone (TRH) seems to be reduced in patients in critical clinical condition. There is evidence that in certain periods of severe disease there may be genuine central and transient hypothyroidism, in which there is not a nighttime peak in TSH, as well as evidence of changes in the glycosylation process regulated by TRH.…”

“…There is evidence that in certain periods of severe disease there may be genuine central and transient hypothyroidism, in which there is not a nighttime peak in TSH, as well as evidence of changes in the glycosylation process regulated by TRH. 4,9,[19][20][21][22][23][24][25][26][27][28] Studies have also suggested reduced T4 action in tissue levels, varying from tissue to tissue, through the demonstration of low serum levels of angiotensin-converting enzyme, which in turn is stimulated by thyroid hormones. 5,7,[20][21][22][23][24][25][26][27][28] In the recovery phase, there may be a temporary increase in TSH.…”

“…4,9,[19][20][21][22][23][24][25][26][27][28] Studies have also suggested reduced T4 action in tissue levels, varying from tissue to tissue, through the demonstration of low serum levels of angiotensin-converting enzyme, which in turn is stimulated by thyroid hormones. 5,7,[20][21][22][23][24][25][26][27][28] In the recovery phase, there may be a temporary increase in TSH. [20][21][22][23][24][25][26][27][28] High T4 syndrome This is characterized by high serum levels of T4, normal or slightly increased T3 and high reverse T3.…”