Prenatal treatment with thyrotrophin releasing hormone to prevent neonatal respiratory distress.

Three major strategies, that are not mutually exclusive, are being developed to tackle the problem of respiratory distress syndrome in preterm infants. The first is to prevent premature birth itself through improved obstetrical follow up and care; however, this has proved not to be an easy task.' The second is to optimise the postnatal treatment of infants with respiratory distress through the availability of neonatal intensive care units and their motorised or airborne transportation teams, as well as through the use of novel medication and techniques, for example, the endotracheal administration of biosynthetic pulmonary surfactant, artificial ventilation with liquid or high frequency oscillation, and extracorporal membrane oxygenation. The third strategy is to administer, in cases of threatening premature birth, a treatment to the fetus that accelerates the fetal preparation for neonatal respiration, thus preventing the development of neonatal respiratory distress. The concept of accelerating fetal maturation was launched in 1969, when Liggins noted as an epiphenomenon of his study on the initiation of parturition in the ewe that the infusion of dexamethasone had a stimulatory effect on the lung aeration of prematurely delivered lambs.2 This pioneering observation has now been repeatedly confirmed and has been extended to numerous miammalian species, including the human. In addition, the underlying pathophysiological mechanisms are increasingly well understood.3 The principle has been applied successfully in human perinatal medicine, where the administration of glucocorticoids to the pregnant woman-and thus transplacentally to the fetus-has served as the 'gold standard' of fetal maturational treatment for nearly two decades.4 5 The regulation of lung development during fetal life has been documented extensively to be under multihormonal control.3 Thyroid hormones in particular appear to stimulate fetal pulmonary maturation. However, as thyroid hormones and thyroid stimulating hormone (TSH or thyrotrophin) fail to cross the human placental barrier sufficiently,6 thyrotrophin releasing hormone (TRH) has become the prime focus of attention.7 There is evidence suggesting that TRH may also be useful in accelerating fetal maturation through its nonendocrine actions.