Thyroxine fetal

MMI and PTU can lead to methimazole embryopathy with choanal or esophageal atresia. In pregnant women the antithyroid diug dose should be minimized to prevent fetal hypothyroidism by maintaining the maternal free thyroxine serum level slightly above the upper limit of normal. 

Hypothyroid women frequently have anovulatory cycles and are therefore relatively infertile until restoration of the euthyroid state. This has led to the widespread use of thyroid hormone for infertility, although there is no evidence for its usefulness in infertile euthyroid patients. In a pregnant hypothyroid patient receiving thyroxine, it is extremely important that the daily dose of thyroxine be adequate because early development of the fetal brain depends on maternal thyroxine. In many hypothyroid patients, an increase in the thyroxine dose (about 30-50%) is required to normalize the serum TSH level during pregnancy. Because of the elevated maternal TBG levels and, therefore, elevated total T4 levels, adequate maternal thyroxine dosages warrant maintenance of TSH between 0.5 and 3.0 mll/L and the total T4 at or above the upper range of normal. 

Thyroid hormones Thyroxine Thyroid gland Fetal brain and bone development, oxygen consumption, gut motility... 

And why is it that, while we could evoke these enzymes by cortisol (e.g. alanine aminotransferase) or thyroxine (malic enzyme) in neonatal life, we could not do so prenatally The explanation can clearly cannot lie in receptor availability since the same hormones do induce alternative enzymes at the same fetal stage. 

There is thus ample evidence supporting the idea that GH regulates somatomedin C levels. In many respects it appears to be the major factor affecting these levels, but it should be stressed that other hormones (including thyroxine and insulin) and nutritional factors are also of considerable importance. The effects of GH on IGF-II levels are less important than those on somatomedin C placental lactogen may be more important here, in partial accordance with the idea that IGF-II is concerned particularly with the regulation of growth of fetal tissues. 

The thyroidogenic effects and corresponding biochemical mechanisms of PCBs and other OHS were recently reviewed by Brouwer et al. [44]. The selective retention of certain OH-PCB congeners in blood (Sect. 5.2.2 and 5.3.2) is concomitant with effects observed on the plasma levels of thyroid hormones. Thyroxine is transported in plasma by a protein complex consisting of TTR and retinol binding protein (RBP). Rats administered CB-77 were shown to have reduced plasma levels of both thyroxine and retinol [196]. A major metabolite of CB-77, 4-OH-3,3, 4, 5-tetrachlorobiphenyl, was identified as the active compound [40]. The same hydroxy-PCB metabolite was found to be retained in mouse fetal soft tissue [191,197]. 

Administration of 4-OH-3,3, 4, 5-tetrachlorobiphenyl and 4-OH-CB107 to pregnant mice reduced the total thyroxine levels in both maternal and fetal plasma [34]. However, the decrease was less dramatic when the CB-77 was administered alone, and the metabolite formed in vivo [197]. Administration of Aroclor 1254 to adult rats resulted in high OH-PCB levels in plasma and a concomitant reduction in thyroxine [198]. In fetal and weanling rats, similar... 

OH-PCBs can also influence thyroxine metabolism. Some of the OH-PCBs that are retained in blood were shown to strongly inhibit sulfation of thyroxine in vitro [204-206]. As sulfation is a major regulation pathway of thyroxine in the fetus, the OH-PCBs may negatively influence the development of the fetus, and in particular fetal brain development [44]. Diodinase mediation is another pathway for thyroxine metabolism e.g., to the active hormone triiodothyronine. Hydroxylated metabolites of CB-77 were shown to inhibit triiodothyronine formation in an in vitro assay using rat hepatic microsomes [207],... 

United Nations to alleviate iodine deficiency. Iodine is required for the thyroid hormones, thyroxine and triiodothyronine, that regulate the metabohc rate and O2 consumption of cells. Iodine is also intimately involved in the control of growth and development, particularly during fetal and infant life. 

Various maternal metabolic dysfunctions can cause fetal cerebral palsy. An example is maternal iodine deficiency and resulting hypothyroxinemia (abnormally low concentration of blood thyroxine). 

Amiodarone may cause asymptomatic corneal microdeposits and inhibit the conversion of thyroxine (T4) to triiodothyronine (T3). Amiodarone has caused pulmonary toxicity (hypersensitivity pneumonitis or intershtial/alveo-lar pneumonihs). It is embryotoxic in that it increases fetal resorphon and causes growth retardation. Amiodarone is excreted in breast milk. 

The thyroid gland synthesizes and releases T3 (3, 3 -triiodothyronine) and (thyroxine) which regulate protein synthesis, regulate membrane-bound enzymes and stimulate mitochondrial oxidation. T3 and also regulate fetal and infant brain development and childhood growth. T3 is more potent than T. ... 

In another critical study, it was observed that thyroid hormone does indeed cross the placenta. Therefore, if insufficient iodine is available to the mother it results in reduced maternal synthesis of thyroid hormone with insufficient placental thyroxine transport for fetal requirements. 

Adequate maternal thyroxine concentration is essential for fetal nervous system maturation. 

The fetal thyroid gland begins its hormonal production after 10 weeks of gestation, when many thyroxin-dependent... 

Figure 63.1 The figure shows fetal thyroxinemia and the development of thyroxine-dependent organs. Maternal thyroxine Is essential for the neurological development of the fetus.

Most studies show that iodine deficiency and maternal—fetal hypothyroxinemia have negative effects on fetal neural maturation, dendritic arborization and synaptic formation. It also significantly delays axonal myelinization and gfio-genesis, which starts at the third trimester and accelerates in the postnatal period. Recent studies have clearly demonstrated the necessary role of maternal thyroxine in early neurogenesis (de Escobar et al., 2004 Bernal, 2005). 

After the initiation of fetal thyroxine synthesis, transfer of thyroid hormones from the mother to the fetus does not stop, but continues until birth. During that period, 20—50% of cord serum thyroxine is composed from maternal supply (de Escobar et aL, 1990 Vulsma et ai, 1989). Several clinical syndromes attributable to iodine deficiency vary according to the timing and the severity of the deficiency. It has been shown that neurodevelopmental disorders in... 

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