cosyntropin and Placenta-Diseases

Diminished total plasma cortisol levels have been demonstrated in postmature neonates, suggesting that fetal glucocorticoids may be involved in the cause of postmaturity. This hypothesis was tested by adrenocortical stimulation in 32 newborns: 12 were postmature; 12 were postterm, but not postmature; and 8 were normal term neonates. The mean pre- and poststimulation total plasma cortisol levels were 3.9 and 50.9 microgram/100 ml, respectively, for the postmature newborns, 9.7 and 44.0 microgram/100 ml for the postterm, but nonpostmature newborns, and 9.8 and 37.1 microgram/100 ml for the normal term newborns. The differences in the poststimulation rise in plasma cortisol between the postmature and merely postterm infants or between the postterm and normal term infants were not statistically significant. The mean poststimulation cortisol rise in the postmature group exceeded that of the normal term group (P less than 0.05). The adequacy and promptness of response to adrenocortical stimulation eliminate the likelihood of adrenal insufficiency in postmature infants.

Topics: Adrenal Cortex; Adrenal Cortex Diseases; Adrenocorticotropic Hormone; Cosyntropin; Female; Humans; Hydrocortisone; Infant, Newborn; Placenta Diseases; Pregnancy; Pregnancy, Prolonged