Pregnancy 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. 

The above-mentioned facts form the basis of a new concept of the adverse effects of not only maternal hypothyroidism, but also maternal hypothyroxinemia without overt hypothyroidism, on fetal brain development. This concept focuses on the necessity for therapeutic correction of maternal hypothyroxinemia detected in pregnancy. MRS, a quantitative laboratory and imaging technique, may be used to show the effects of hypothyroxinemia due to iodine deficiency and its correction in the human brain in an objective manner. 

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. 

Hypothyroxinemia is a condition characterized by normal TSH concentrations but maternal free-thyroxine concentrations that are below the normal range for the stage of pregnancy. 

It occurs in very specific environmental and/or physiological circumstances, namely ID and pregnancy. The coexistence of both of these conditions, i.e. pregnancy in women whose iodine intake is inadequate, results in the highest risk of gestational hypothyroxinemia in the mothers. 

Reduced Iodine Intake and Iodine Prophylaxis in Pregnancy Importance of Hypothyroxinemia in the First Trimester of Gestation... 

The importance of the transfer of thyroid hormones from the mother to the fetus during the second half of pregnancy in humans has received increasing attention (Burrow et ai, 1994). Recently, it has become evident that maternal hypothyroxinemia results not only in the birth of children with neurological cretinism, but also in decreased mental and psychomotor development of the rest of the population without cretinism (Beichrodt and Born, 1994). 

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. 

Hypothyroxinemia in pregnancy should be diagnosed as soon as possible, and is recommended before 12 weeks of gestation. 

Hypothyroxinemia diagnosed during pregnancy should be treated immediately with administration of levothyroxine. 

Nishiyama et al. (2004) Observational study Japan Association of hypothyroxinemia and persistent hyperthyrotropinemia in neonates with excessive intake of kombu, other seaweeds and instant kombu soups by the mothers during pregnancy... 

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

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). 

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