Properties of thyroid-stimulating hormone and cortisol secretion by the human newborn on the day of birth.

Secretory activation of the thyroid and adrenal glands is a hallmark of the neonatal adaptation to extrauterine life. TSH and cortisol play key roles in these axes. The highest serum concentrations of TSH attained over the full span of human life are normally found shortly after birth. Serum cortisol is also known to be elevated in the immediate postnatal period. However, the dynamics of TSH and cortisol secretion have hitherto not been documented on the day of birth. To study the properties of neonatal TSH and cortisol secretion, we obtained arterial blood at regular intervals (every 20 min for 6 h) from nine polycythemic newborns (gestational age, 34-41 weeks) on the first and/or fourth days after birth during a therapeutic, standardized, isovolumetric, partial exchange transfusion. One premature infant had received betamethasone antenatally. The serum TSH level of an infant with congenital hyperthyroidism of transplacental origin was also measured at the postnatal age of 1 h. Deconvolution analysis of the profiles revealed that all infants displayed a combination of basal and pulsatile TSH release. Bursts of TSH secretion occurred at a median interval of 133 min. The median serum TSH half-life was 75 min. On the day of birth, basal TSH secretion and the amplitude of pulsatile TSH secretion were higher than 3 days later. Cortisol was secreted exclusively in a pulsatile fashion. Bursts of cortisol release occurred at a median interval of 69 min. The median serum cortisol half-life was 60 min. Cortisol secretion appeared to shift gradually from a high frequency, low amplitude pattern early on the first day toward a lower frequency, higher amplitude pattern 3 days later. TSH and cortisol secretion were low in the infant who received betamethasone prenatally. Serum TSH was undetectable in the infant with congenital hyperthyroidism. In conclusion, serum TSH concentrations in the human newborn appear to be elevated on the day of birth as a result of amplified basal and pulsatile TSH release, then fall rapidly through a mechanism that decreases the amplitude of TSH secretion and are affected by modulation of the fetal thyroid axis. From the day of birth onward, cortisol was found to be released in an exclusively pulsatile mode, with characteristics that appear to depend on postnatal age and prenatal glucocorticoid exposure.