Maternal-fetal thyroid hormone

Alterations of Maternal-Fetal Thyroid Hormone Metabolism Induced by Iodine Excess... 

It was concluded that both maternal and fetal thyroid hormones were involved in the effect of iodine deficiency... 

Iodine and thyroid hormones affect all stages of human development, from in utero life to adulthood. Iodine deficiency leads to insufficient production of thyroid hormones, which play a vital role in the process of early growth and development of many organs. During pregnancy, both maternal and fetal thyroid hormones are required for normal fetal brain development. Of them, maternal hormones constitute the main source in the first and the second trimesters, whereas the contribution of fetal hormones becomes more important in the third trimester (de Escobar et aL, 1985 Vulsma et ai, 1989). Many studies indicate that iodine deficiency and iodine-induced maternal-fetal hypothyroxinemia result in impairment of central nervous system (CNS) development during fetal and early postnatal life. 

These observations suggested that normal brain development requires the availability of both maternal and fetal thyroid hormones,a suggestion which is at variance with earlier reports (9) (14) (15) (16) that the placenta in many mammalian species is relatively impermeable to thyroid hormones and with the suggestion (17) (18) that early mammalian development takes place normally in the absence of thyroid homrones. The observations do agree however with a more recent report (19) that rat embryonic tissues are provided with T and T3 only four days after uterine implantation and well before the onset of fetal thyroid function at 17 days. y also supported by the work of Woods et al (20) who showed that T and T3, when injected into pregnant rats, entered the rat... 

This is further indicated by evidence of the relation of maternal thyroxine levels to the risk of cretinism and the psychomotor defect from studies in Papua New Guinea (26). The subsequent lack of fetal thyroid hormones due to the inadequate supply of iodine in iodine deficiency would exacerbate the effects of maternal thyroid insufficiency and the combination of effects, which were represented experimentally in the sheep by maternal thyroidectomy before conception (21) combined with fetal thyroidectomy at 98 days (12), might be expected to produce the multiple defects of neurological cretinism. 

As regards the second question, results described here might afford a possible explanation for the adverse effects of maternal hypothyroxinemia on the CNS of the progeny, even if maternal T3 levels are normal. This is a frequent finding in v/omen with severe iodine deficiency "" . If production of fetal thyroid hormones is impaired because of inadequate iodine supply, and the mother also has very low plasma T4, the brain would be totally deprived of T3, despite marked increases in cerebral 5 D-II. The normal maternal plasma T3 levels cannot mitigate this cerebral T3 deficiency, because the T3 transferred from the mother does not enter the fetal brain. However, the normal maternal levels of T3 might afford some protection to other fetal tissues, which would be in a better situation than if maternal T4 and T3 were both low. This might also explain why at birth babies from... 

Adverse reproductive effects have been observed in animals fed PCB in the diet. Fetal resorptions were common, and dose-related incidences of terata were found in pups and piglets when females were fed Arochlor 1254 at Img/kg/day or more. Long-term low-level maternal exposure of rats before breeding and throughout gestation and lactation caused permanent hearing deficits, decreased serum thyroid hormones, and reproductive effects. PCBs have been observed in human cord blood and in tissues of newborn humans and animals. ... 

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. 

The transplacental passage of maternal iodothyronines is quantitatively modest, although it might be sufficient to ensure adequate fetal development. Maternal thyroid hormone secretion is markedly increased during pregnancy (by 25-50%) thyroid therapy should therefore be carefully adjusted during pregnancy (58). 

Most proteins Thyroid hormones Maternal IgM, IgA Maternal and fetal erythrocytes... 

A deficiency of thyroid hormone during fetal development due to untreated or undertreated maternal hypothyroidism results in a neurological deficit in the offspring. In congenital hypothyroidism, a normal maternal thyroid can meet the fetal requirements for thyroid hormone. However, in the postnatal period these infants require a prompt thyroid hormone replacement therapy throughout their life, beginning in the first few weeks of life. If untreated, they inevitably develop growth and mental retardation. Thyroid hormone is essential for maturational development of the CNS and is required for the development of axonal projections and myelination. One of the important effects of thyroid hormone is to promote the synthesis of myelin basic protein. 

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. 

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