Thyroid hormone relationships between maternal and fetal circulations in human pregnancy at term: A study in patients with normal and abnormal thyroid function

Abstract Determinations of the protein-bound iodine (PBI), resin-T3 uptake (R-T3), free thyroxine (FT4), and free thyroxine index (FT4-Ix) were made in paired sera from 97 mothers and the umbilical cords of their respective infants. These parameters were categorized into six groups according to the clinical thyroid status of the mother. While maternal and cord PBI values in the normal group were not significantly different, serum levels of FT4 and FT4-Ix in the same cord sera were each significantly higher than their respective maternal values. Results of similar determinations in other groups were variable, but statistical analyses of these data were interpreted to indicate that wide maternal variations in these parameters could occur at term in the absence of corresponding fetal alterations. Activation of the fetal pituitary-thyroid axis may be initiated by a decrease in placental permeability for thyroxine near term. Diminished transfer of maternal thyroid hormones to the fetus would thus result in a transient fall in fetal serum and tissue levels with resultant secretion of fetal thyroid-stimulating hormone (TSH). A relative placental impermeability at term would also limit potential reflux of fetal thyroid hormones to the mother. From a conceptual viewpoint, this series of events occurs in anticipation of fetal pituitary-thyroid autonomy at birth.