Neonatal Thyroid Function

Abstract

Postnatal changes in thyroid hormone economy reflect the adjustment of the fetus to the extrauterine environment. Thyroid-stimulating hormone (TSH) surges soon after birth, resulting in thyroxine (T4) concentrations that are higher in the first postnatal week than at any other time of life and in circulating triiodothyronine (T3) concentrations that are three to four times higher than in the fetus. In preterm infants born after 31 weeks' gestation, the pattern is similar, although less pronounced; in younger infants, a decrease in TSH may be seen, accompanied by a low T4 concentration. Usually the free T4 concentration is less affected than the total T4. Thyroid hormone synthesis is critically dependent on an adequate prenatal and postnatal supply of iodine, which can paradoxically suppress T4 secretion when present in excess, especially in preterm infants and in the presence of iodine deficiency. Maternal T4 is a critical source of thyroid hormone when the fetus is hypothyroid. Postnatal thyroid function also can be affected by maternally or postnatally administered drugs, maternal TSH receptor antibodies (Abs), and acute illness. Because of the vital role of thyroid hormone in brain development and the importance of early, adequate therapy when thyroid function is impaired, knowledge of normal thyroid function in the neonatal period and factors affecting it are critical for physicians caring for newborns.