The fact that neonates who subsequently have severe hypothyroidism have no evidence of the condition at birth suggests the possibility of the placental transfer of thyroid hormones. Recent studies have demonstrated the existence of such transfer in hypothyroid rats. To determine whether there is a transfer of thyroxine (T₄) from mother to fetus, we studied 25 neonates born with a complete inability to iodinate thyroid proteins and therefore to synthesize T₄. This total organification defect is an autosomal recessive disorder with an incidence of approximately 1 in 60,000 neonates in the Netherlands.

In the cord serum of affected neonates, T₄ levels ranged from 35 to 70 nmol per liter. Since these patients were unable to produce any T₄, the T₄ must have originated in their mothers. The estimated biologic half-life of serum T₄ was 3.6 days (95 percent confidence interval, 2.7 to 5.3). In 15 neonates with thyroid agenesis, the serum levels and the disappearance kinetics of T₄ were the same as those in the neonates with a total organification defect, suggesting that in these infants, the T₄ also had a maternal origin.

We conclude that in infants with severe congenital hypothyroidism, substantial amounts of T₄ are transferred from mother to fetus during late gestation. (N Engl J Med 1989;321:13–6.)