III. Immaturity of the lungs: neonatal perspective - could we influence the fetal lung maturity?

Abstract

Could we influence the fetal lung maturity? Many experimental and clinical studies can give us a positive answer. It is well known that fetal lung maturation is affected by a number of hormones and pharmacological agents, including adrenocorticotropic hormone (ACTH), glucocorticoids, thyrotropin-releasing hormone (TRH), and tri-iodothyronine (T₃); agents influencing the intracellular content of cyclic adenosine monophosphate (cAMP), such as beta-adrenergic agonists and aminophylline; substances increasing intracellular calcium or acting on protein kinase C, etc.

Full Text

Could we influence the fetal lung maturity? Many experimental and clinical studies can give us a positive answer. It is well known that fetal lung maturation is affected by a number of hormones and pharmacological agents, including adrenocorticotropic hormone (ACTH), glucocorticoids, thyrotropin-releasing hormone (TRH), and tri-iodothyronine (T₃); agents influencing the intracellular content of cyclic adenosine monophosphate (cAMP), such as beta-adrenergic agonists and aminophylline; substances increasing intracellular calcium or acting on protein kinase C, etc. But the only currently well-established agent for improving pulmonary as well as others outcomes for the preterm infant is antenatal glucocorticoid administration. Many of controlled clinical trials confirm that glucocorticoids are indicated in women with preterm labor between 24 and 34 weeks gestation, or after 34 weeks if studies show that the fetal lung is immature, but they must be administered at least 24 to 48 hours before delivery. 12 mg of betamethasone (or dexamethasone) in two doses every 24 hours for 3 consecutive days is recommended. The possibility of combining glucocorticoid with TRH antenatally, with appropriate administration of surfactant replacement at birth, is very promising.