Alterations in the thyroid metabolism of hypoxic, fasted, and chronically ill adults and older children have been described. We evaluated the effects of asphyxia on thyroidal indices of term newborns and compared them to those of a control population. Blood was drawn from the cord and then serially at 5 min and 3, 24, and 48 h after delivery in all patients. Seven term healthy newborns (group 1)increased their free thyroxine (FT4) concentrations significantly after delivery from a mean +/- SD baseline of 0.94 +/- 0.13 ng/dl in cord blood to a mean +/- SD peak of 2.6 +/- 0.6 ng/dl 48 h after delivery (p less than 0.001 at 3, 24, and 48 h), while their free triiodothyronine (FT3) levels increased from a mean +/- SD baseline level of 2.3 +/- 0.5 pg/ml in cord blood to a mean +/- SD peak of 3.7 baseline level of 2.3 +/- 0.5 pg/ml 48 h after delivery (p less than 0.001 at 24 and 48 h). Seven term newborns with transient low Apgar scores at birth (group 2) and seven term neonates born to mothers with toxemia or hypertension (group 3) failed to increase their FT4 and FT3 concentrations above baseline during the first 48 h of life. FT4 and FT3 values at 3, 24, and 48 h were significantly higher in the control group than in groups 2 and 3. Cord blood thyroid-stimulating hormone, FT4, and FT3 levels were not statistically different in the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

The growth hormone response to a single intravenous dose of human growth hormone-releasing hormone (GHRH) was examined in 23 healthy neonates (12 term and 11 preterm) aged 2–4 days. There were no significant increases in growth hormone concentrations at any point in time studied following GHRH administration in either group of new-borns. The mean basal growth hormone levels of term neonates were significantly higher than those of the premature newborns (39.6 ± 5.3 vs. 23.2 ± 3.3 ng/ml; p < 0.01) and this difference in growth hormone remained significant 15 and 30 min after GHRH injection. Gestational age correlated positively with both basal and peak growth hormone concentrations in our patients. In conclusion, first, neonates studied in their first days of life have high basal levels of growth hormone and fail to further secrete any significant amount of growth hormone following a single dose of GHRH, and, second, premature newborns secrete significantly less growth hormone than do term neonates.

To evaluate whether the hypothyroxinaemia, previously noted in hyperbilirubinaemic newborns immediately after exchange transfusion for Rh or AB0 incompatibility, was due to impairment in the secretion of thyroid stimulating hormone (TSH) by the pituitary, we studied the thyroid hormone response to thyrotropin releasing hormone (TRH) and compared this response to that seen in a control population of healthy neonates. All infants studied responded with a brisk TSH increase; 30 min after TRH injection the mean TSH concentration of the hyperbilirubinaemic patients was 37 microU/ml, ten times their basal level, which was not different from the value noted in the control population. No significant change in total thyroxine (T4), 3,5,3' triiodothyronine (T3), free thyroxine (FT4) or 3,3',5' triiodothyronine (rT3), (FT4) or (rT3) was noted after TRH administration in either group of neonates. In addition the effect of exchange transfusion on the thyroid axis of hyperbilirubinaemic newborns was evaluated. Before the exchange transfusion TSH, T4, rT3, T3 and FT4 levels were higher in the hyperbilirubinaemic newborns than in donor blood; immediately post-exchange transfusion TSH and T4 concentrations of the hyperbilirubinaemic neonates decreased significantly and remained significantly below pre-exchange values 30 h later. Newborns undergoing an exchange transfusion respond appropriately to TRH stimulation and seem to have an intact pituitary-thyroidal axis.