Pregnancy early maternal hypothyroxinemia

The neurological abnormalities observed in neurological cretinism seem to be caused by maternal hypothyroxinemia during the first period of brain development, early in pregnancy. In iodine deficiency the maternal plasma T4 is low, even if plasma T3 and TSH are normal. 

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. 

Maternal hypothyroxinemia is not detected in most pregnant women early in pregnancy, since it does not necessarily result in cfinical or subcfinical hypothyroidism. The mother herself may synthesize and secrete enough T4 and T3 to meet her own needs, but the amount of T4 reaching the fetus might not be sufficient for normal neurodevelopment. 

In addition, data collected in rats showed that maternal hypothyroxinemia results in fetal hypothyroxinemia and brain damage during early pregnancy, even before the onset of fetal thyroid function (75-81). 

Zoeller and Rovet (2004) summarized the models of maternal hypothyroidism, hypothyroxinemia and CH. If TH deficiency occurs early in pregnancy, the children... 

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