MATERNAL-FETAL T(4)-TRANSFER DOES NOT SUFFICE TO PREVENT THE EFFECTS OF IN-UTERO HYPOTHYROIDISM

It has been suggested recently that in congenitally hypothyroid infant s with organification defect there is a maternal-fetal transfer of thy roxine (T4). The present study was conducted to evaluate how effective the maternal-fetal transfer is and whether the maternal T4 can preven t intrauterine hypothyroidism. The clinical, laboratory and radiologic al data on 271 full-term infants with persistent primary congenital hy pothyroidism, detected by the national screening program, were used to assess the degree of in utero hypothyroidism. For 6 out of 50 athyroi d infants, two pretreatment blood samples spotted on filter paper were available for calculating the T4 disappearance rate. Most infants wit h agenesis of the thyroid had very low T4 and very high levels of thyr oid-stimulating hormone compared to infants with ectopic thyroid. In t he athyroid infants the initial T4 declined to low and undetectable le vels. Bone maturation was significantly delayed while the clinical sym ptomatology was more prominent in the athyroid congenital hypothyroid infants, as compared with the ectopic thyroid infants. In conclusion, there is some maternal-fetal transfer of T4. However, this transfer is insufficient to suppress the fetal levels of thyroid-stimulating horm one and prevent intrauterine hypothyroidism.