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Respiratory distress syndrome (RDS) is the main cause of death among premature newborn infants [21]. Despite recent improvements in treatment by neonatal intensive care and respiratory assistance, mortality from RDS remains high [20]. Inadequate pulmonary surfactant is thought to be a primary factor leading to the development of RDS [2]· LIGGINS [12] was the first to observe an accelerated lung maturity of fetal lambs treated in utero with glucocorticoids. LIGGINS and HOWIE [14] first reported the beneficial effect of the maternal administration of antepartum glucocorticoid on the incidence of RDS in premature infants. This has since been confirmed by others [3,5,8,18]. However, attention must be drawn to the possibility of an adverse effect of corticosteroid treatment in cases with hypertensionedema-proteinuria syndromes. In this group a significantly higher fetal death rate was observed under betamethasone therapy [13]. Studies indicating a high incidence of RDS in neonatal hypothyroidism [25] suggest the possibility that thyroid hormones may play an important role on fetal lung maturation. Several animal studies have suggested an important influence of thyroid hormones on acceleration of lung maturation and enhancement of surfactant production [22,27]. Curriculum vitae

Intraamniotic Triidothyronine instillation for prevention of respiratory distress syndrome in pregnancies complicated by hypertension