Antenatal glucocorticoid has proven to be one of the most successful single therapeutic approaches for preventing serious consequences after preterm birth. The fetal compartment is protected against endogenous corticosteroid by the high endogenous 11β-hydroxysteroid dehydrogenase type 2 that converts cortisol to cortisone and by the poor responsiveness of the fetal hypothalamus to corticotropin-releasing hormone. High corticosteroid activity acutely enhances the functional maturity of the fetus. Persistently high fetal glucocorticoid activity has adverse effects on the growth and differentiation of the fetal brain and other organs. Intrauterine growth restriction may be associated with high fetal glucocorticoid activity. Antenatal glucocorticoid therapy which is aimed to be given within 1-10 days before preterm birth is likely to increase the success of postnatal noninvasive treatments of very preterm infants.

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