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The best treatmentof respiratory distress syndrome (RDS) is preventive. The occurrence of the syndrome can be lessened by the antenatal assessment of fetal lung maturity, thus leading to an improved selection of pregnancies for induction. Parallel to this passive management many efforts have been made to accelerate the physiological synthesis of pulmonary surfactant. LIGGINS and Howrn [8] were the flrst to demonstrate a decrease in RDS in premature infants by the antenatal administration of Be tarne thasone to the mother. Since then other corticosteroids and other routes of administration have also come into use [2, 17]. Due to the theory that the increase in the phospholipid component of surfactant may be mediated by thyroxine, its use for accelerating fetal lung maturity has been tested. Experimental studies in rats and rabbits have demonstrated the effect of thyroxine in accelerating fetal lung maturity [11, 18].' In humans thyroxine has been injected into the amniotic sac for other purposes 12-24 hours prior to delivery without any early deleterious effect to mother or newborn [4]. These observations provided the basis for using this hormone in pregnant women in order to accelerate fetal lung maturity. Curriculum vitae

The effect of intraamniotic thyroxine administration on fetal lung maturity in man