Chevalier Jackson Lecture: In quest of the prevention of hyaline membrane disease.

Hyaline membrane disease or respiratory distress syndrome of prematurely born infants is more common in males, in Caucasians, has a familial predisposition, and is associated with maternal diabetes and delivery by cesarean section before the onset of labor. Now known to be the sequel of surfactant deficiency, it can be predicted prenatally by assay of amniotic liquid for surface active materials produced by the fetal lung. Deficiency of adequate surfactant synthesis or secretion can result in low levels of lecithins and other phospholipids in amniotic liquid. Lung maturation can result in low levels of lecithins and other phospholipids in amniotic liquid. Lung maturation can be accelerated if labor or elective delivery can be deferred at least 24 hours. Glucocorticoids given to the mother cross the placenta and enter fetal lung tissues; specific receptors exist in the lung which permit glucocorticoids to promote cell differentiation and surfactant synthesis precociously. Clinical trials support the efficacy and lack of short-term toxicity of glucocorticoids in human pregnancy after 28 weeks gestation in the event of premature onset of labor. Maternal toxemia, infection or illness which may be aggravated by glucocorticoids may contraindicate prenatal treatment. Postnatally endogenous glucocorticoids accelerate lung maturation, and further administration confers no additional benefit.