Effects of antenatal and postnatal corticosteroids on the preterm lung.


It is nearly 25 years since Liggins and Howie first reported the maturational benefits of antenatal corticosteroids given to mothers of preterm infants. They reported reduced incidence of respiratory distress syndrome (RDS) in preterm infants delivered to mothers treated with antenatal steroids. Since then, several other studies have reported similar benefits for antenatal corticosteroids. Indeed, Crowley has reported a meta-analysis of 15 randomised trials, conducted between 1972 and 1994, which studied the use of antenatal corticosteroids in preterm labour. Overall, the incidence of RDS was halved in infants delivered to mothers who had received antenatal corticosteroids compared with those born to mothers treated with placebo. Secondary analysis clearly showed that when antenatal corticosteroids are given between 24 hours and 7 days before delivery, the odds ratio is 0.35 (95% CI 0.26–0.46). This is reduced to 0.8 (95% CI 0.56–1.15) if antenatal corticosteroids are given at less than 24 hours before delivery, and to 0.63 (95% CI 0.38–1.07) if given more than seven days before delivery. Clearly, antenatal corticosteroids require at least 24 hours to exert their eVects. Clinical trials of postnatal systemic corticosteroids in established chronic lung disease of prematurity (CLD) have been thoroughly reviewed by Ehrenkranz and Mercurio. At least nine randomised controlled trials of parenteral or oral dexamethasone have been reported for infants aged 2–6 weeks of postnatal age. All except two 10 were devoted exclusively to intubated babies. The UK collaborative trial, one of the largest with 285 babies, covered a wide clinical spectrum of disease. The main outcome measures in most trials were speed of extubation and duration of oxygen treatment. Extubation was clearly facilitated in all but one study, but the overall duration of oxygen treatment and of inpatient stay were generally unaVected. Although postnatal corticosteroids may facilitate weaning from mechanical ventilation, the optimal timing of treatment is uncertain. Some evidence points to improved benefits if given early. 14 As with antenatal corticosteroids, the mechanisms involved in the improvement in pulmonary function in CLD are currently poorly understood. EVects of corticosteroids on lung growth Studying the specific eVects of corticosteroids on human infants is diYcult because diseases such as CLD may themselves aVect lung growth. 16 Most studies have therefore concentrated on animal models to determine both beneficial and adverse eVects of these drugs on lung growth. When given antenatally, corticosteroids accelerate lung maturation. The normal thinning of the double capillary loops, to form the thin gas exchanging walls of alveoli, is accelerated, resulting in rapid alveolisation. The maturation of surfactant producing type II pneumocytes is also speeded up. Although the alveolisation occurs rapidly as a result of the corticosteroids, the total number of alveoli is decreased. This was reported by Beck et al, who treated preterm Rhesus monkeys (between 66% and 85% of term) with antenatal corticosteroids. This decrease in eventual numbers of alveoli is partly due to suppression of the formation of secondary septa, a necessary step in the division of alveoli. These observations of accelerated alveolisation with ultimate reduction in total number of alveoli has also been reported by Plopper’s group. They also showed decreased body weight in Rhesus monkeys treated with antenatal steroids. This reduction in body weight was most obvious when the drugs were used early in gestation than when given later, and when higher doses of corticosteroids were used. Thus antenatal corticosteroids improve alveolisation in preterm animals at a critical time when delivery may result in severe acute respiratory failure. However, lung growth and body weight may be aVected in the long term by such treatment. The eVects of postnatal steroids are similar and have been proved in some elegant studies by Burri’s group. When dexamethasone was given postnatally to newborn term rats for the first two weeks of life, acceleration of the alveolar wall thinning and microvascular maturation were seen, together with partial suppression of formation of secondary septa. A week after treatment had stopped, the accelerated lung maturation was partially reversed with the inter-airspace septa regressing towards a more immature thickened state. A secondary burst of alveolisation followed, but the eventual result of postnatal corticosteroid treatment was an Archives of Disease in Childhood 1997;77:F147–F150 F147

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@article{Vyas1997EffectsOA, title={Effects of antenatal and postnatal corticosteroids on the preterm lung.}, author={Julian R. Vyas and Sailesh Kotecha}, journal={Archives of disease in childhood. Fetal and neonatal edition}, year={1997}, volume={77 2}, pages={F147-50} }