Numerous trials have confirmed that prenatal glucocorticoid treatment of women threatening preterm delivery increases survival and reduces the occurrence of respiratory distress syndrome, intraventricular haemorrhage and necrotising enterocolitis in infants born before 32–34 weeks’ gestation.1 However, despite widespread use of prenatal steroids and administration of surfactant to treat or prevent respiratory distress syndrome, extremely preterm infants remain at high risk for the development of bronchopulmonary dysplasia (BPD). In two large databases in the USA and Canada, BPD, defined as receipt of supplemental oxygen at 36 weeks’ postmenstrual age, affected about a quarter of very low birthweight infants, approximately a third of infants weighing 750–1000 g and half of those who weighed less than 750 g at birth.2 3

The cause of BPD in susceptible infants is multifactorial. The immature lung is most vulnerable to disruption of alveolar development in the stage before alveolar formation begins (23–26 weeks’ gestation). Factors that increase inflammation in the lung—such as oxygen toxicity, mechanical ventilation-induced trauma from volume and pressure changes, and infection—are associated with the development of BPD. Exposure to chorioamnionitis, with resultant fetal inflammatory syndrome and high levels of circulating proinflammatory cytokines, also places preterm infants at increased risk of BPD.4 5 These data suggest that inflammation has an important role in the pathogenesis of BPD and that the pharmacological modulation of the inflammatory response may be protective.

SHORT-TERM EFFECTS OF POSTNATAL STEROIDS

Observations in the late 1980s suggested that pharmacological doses of corticosteroids (predominantly dexamethasone) given to ventilator-dependent premature infants acutely improved respiratory mechanics and facilitated weaning from mechanical ventilation. Although the numerous randomised controlled trials of corticosteroids to treat or prevent BPD make this one of …