Maternal-fetal thyroid hormone iodine

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. 

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... 

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. 

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... 

Iodine deficiency at any degree of severity causes maternal and fetal hypothyroxinemia. As thyroid hormones of the mother and the fetus must be kept at optimal levels, iodine prophylaxis should be provided, especially in iodine deficient areas. To establish normal fetal brain development, iodine supplementation must be started before pregnancy and should be continued during the gestational period. 

Adequate iodine intake is indispensable to the production of thyroid hormone (TH), which is essential for growth, development and cell differentiation. Iodine excess, as well as iodine deficiency, has adverse effects on health. One of the aims of the present review is to summarize the previous evidence and present the major advances in our knowledge of developmental toxic effects induced by excess iodine in animals and humans. Fetal and maternal thyroid systems interact mainly by means of the placenta. When a mother is exposed to excess iodine, alterations in maternal-fetal TH metabolism occur. Another aim of this review is to discuss the pathway of maternal-fetal TH metabolism influenced by excess iodine. Finally, the present review provides new insights into the molecular mechanism of TH action in skeletal development and highlights the potential regulation of the developmental genes, Hox genes (especially HoxcS), by TH in skeletal development. 

Therefore, based on the above Hmited evidence, we conclude that excess iodine exposure may influence maternal-fetal TH metabohsm by three mechanisms (1) excess iodine affects the maternal hormone thyroid level by inhibition of thyroid function and/or Dl activity (2) excess iodine has an effect on maternal—fetal TH transfer by affecting placental D2 and D3 activity and (3) excess iodine transferred by the placenta has a direct inhibition on the development and function of the fetal thyroid gland (Figure 88.2). 

Thyroid hormones, T3 and T4, have been i cwn to play significant but poorly understood roles in development and differentiation of rodent and human brain (1-7). In the human, disorders of maternal and fetal thyroid function include maternal and secondary fetal iodine deficiency, maternal hypothyroidism or hyperthyroidism, as well eis disorders related to deficient fetal autcxiomous thyroid hormcaie secretion, i.e., goiter or i radic oongenitel hypothyroidism. These disorders are identifiable causes of mental retardation (4, 8, 9, 10), cer ral peilsy (11, 12), and other significant neurological abnormalities (5, 6, 11) ... 

The data suggesting the direct role of elemental iodine on brain development is the observation that correction of iodine deficiency in mothers prevents the emergence of neurological cretinism only if correction takes place before or during early gestation, thus before the onset of fetal thyroid function (83). What we would like to know in greater detail is which parameter is corrected in the human fetus when maternal iodine deficiency is corrected before the onset of fetal thyroid function Is it the fetal deficiency in iodine, in thyroid hormones or in both ... 

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