THE EFFECT OF MATERNAL THYROID FUNCTION ON FETAL THYROID FUNCTION AND DEVELOPMENT*†

Abstract

Maternal hypothyroidism is not commonly the cause of sporadic fetal hypothyroidism. Seventeen mothers of cretins were examined two months to twenty-four years after the birth of their last cretinous child; of these, 12 were euthyroid, 4 were probably euthyroid and 1 was moderately but definitely hypothyroid. In newborn living pups of dogs thyroidecto-mized during pregnancy, the serum PBI level, thyroidal I131 uptake and thyroid weight in proportion to body weight did not differ from those in pups born of euthyroid dogs. Maternal hyperthyroidism produced by administration of large doses of hormone may, however, lead to significant transplacental passage of thyroid hormone to the fetus. Two mothers who had each previously given birth to 2 cretins were treated with large doses of desiccated thyroid during their third pregnancies. Each gave birth to a living infant whose clinical appearance, bone maturation, cord-blood PBI and BEI concentrations, and thyroidal I131 uptakes suggested that an adequate amount of thyroid hormone had been received transplacentally. Subsequent thyroidal I131 uptakes after administration of TSH suggested that one of the infants was athyrotic. whereas the other had an apparently normal gland temporarily suppressed by the exogenous hormone. Reasons for believing that the athyrotic infant may have a better prognosis for mental development than cretins born of mothers euthyroid during pregnancy are discussed. Experiments in pregnant dogs fed large amounts of thyroxine also suggest some transplacental transfer of thyroid hormone when the maternal concentration of serum PBI reaches very high levels.