Long-term effects on the child of near-term glucocorticoids in the fetus.

Abstract

The human fetal hypothalamic-pituitary axis (HPA) becomes activated as pregnancy advances towards term. This critical developmental trigger occurs in most mammalian species and results in a fetal adrenal glucocorticoid (GC) surge essential for lung maturation[1]. In addition, HPA activation also contributes to parturition and the maturation of other fetal organs. Precocious activation of GC receptors can be induced by endogenous cortisol release in response to fetal exposure to an adverse intrauterine environment, or when synthetic glucocorticoids are administered to the mother during pregnancy (antenatal maternal glucocorticoid, AMGC).