Abstracts Respiratory distress syndrome (RDS) and its complications are a key factor of mortality and morbidity in preterm babies. Premature infants whose mothers received corticosteroid treatment before delivery are less developing RDS and its complications. The mechanism of activity of corticosteroids includes increased fetal production of corticos-teroids, increased conversion of inactive 11-oxysteroid to active 11-hydroxysteroid by target tissues and increased concen-tration of glucocorticoid receptors. Morphologically, the airspace epithelial cells of lung treated with corticosteroids are identical to mature type II cells of adult lung. Fluorinated corticosteroids (dexamethasone, betamethasone) are the only efficient corticosteroids with advantage of a low mineralocorticoid activity. Dexamethasone crosses the placenta to the fetus. The drug is partially metabolized (54%) by the perfused placenta to its inactive 11-ketosteroid derivate, more so than betamethasone, but the difference is not statistically significant. Treatment consists of two doses of betamethasone 12 mg given intramuscularly 24 hours apart or four doses of dexamethasone 6 mg given intramuscularly 12 hours apart. Optimal benefit begins 24 hours after initiation of therapy and lasts 7 days. The risk associated with repeated steroid exposure have not been defined but are probably greater than one course of therapy. The results of Dexamethasone application to 100 pregnant patients are presented.