Thyroid function in the critically ill newborn and child

Abstract

At present, there is no evidence of benefit in giving thyroid hormone to patients with nonthyroidal illness who have low serum T3 or T4 concentrations, including preterm infants and postcardiac surgery patients.

Relationships between thyroid hormones and serum energy metabolites with different patterns of postpartum luteal activity in high-producing dairy cows

“…Unlike T 4 , which is produced solely in the thyroid gland, ,80% of circulating T 3 is produced by extrathyroidal conversion of T 4 to T 3 by 5 0 -deiodinase present in organs such as the mammary tissue (Capuco et al, 2001), liver and kidney (Laurberg et al, 2007;Shih and Agus, 2009). Thus, there are two mechanisms by which T 3 production in cows with AOV may be reduced: decreased activity of the 5 0 -deiodinase that convert T 4 to T 3 and decreased delivery of T 4 substrate for conversion to T 3 .…”

Low free triiodothyronine levels in mexican pediatric population with congenital heart disease after cardiac surgery undergoing cardiopulmonary bypass.

“…The excess and the deficit of thyroid hormones determine pathological states clinically well defined. [6][7][8][9]13 Derangement in all thyroid hormones levels (including thyroid stimulating hormone) has been described elsewhere; however, changes in T3 and specially in free T3 levels are probably the most important, not only for their clinical relevance, but also due to the fact that their reduction have been documented early and in a constant pattern in previous studies. 4,6,9,[13][14][15] Postoperative low levels of T3 and FT3 have been related to adverse postoperative outcomes, with significant increases in IH-LOS, use of inotropic drugs and mechanical ventilatory support requirements in every type of cardiac surgery with CBP.…”

“…[2][3][4][5] Sick euthyroid syndrome, a state related to stress conditions as in shock, severe trauma, and different surgical procedures, has also been associated with the use of CPB in children and adults. 2,4,[6][7][8][9] Variables as age, nutritional status, CPB time, complexity of heart' malformation and the presence of associated genetic syndromes, have been found to be related with the development of PLFT3; its incidence in different series, varies from 10 to 30%. 6,7,9 We report the prevalence of PLFT3 after congenital heart surgery and CPB in our population.…”

“…Their effect on the cardiovascular system depends on genetic and non-genetic factors and they involve the modification of the expression of beta-receptors in myocardium, the stimulation of proteins associated to calcium such as SERCA (sarcoplasmic reticulum calcium ATPase) and the inhibition of its counter-regulatory hormone fosfolambam. 6,7,8 Their effects in blood vessels, seem to be due to the release of other vasodilator substances, within the endothelium, in response to the increase of metabolic rate and oxygen consumption. Simultaneously, there is a direct effect of the hormone on the pulmonary vasculature, which induces an after load reduction, and at the same time, an increase in preload by increasing venous return, with a positive effect on cardiac output and systemic perfusion.…”

“…Our results coincide with those reported in the literature. 4,5,[7][8][9]15 Actually different protocols have been developed to treat PLFT3, all of which have shown an improvement of the levels and the affected variables. However, due to the high cost of intravenous treatment, research is still going on to find the best way to deliver the hormone.…”