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More than five decades ago, Northway et al1 described the clinical, radiological and pathological features of a chronic lung disease in preterm infants characterised by lung emphysema, fibrosis, pulmonary vascular remodelling and cardiac hypertrophy.1 At that time, this chronic lung disease of prematurity, which they named bronchopulmonary dysplasia (BPD), was thought to occur as a consequence of postnatal events, including severe respiratory distress syndrome, oxygen toxicity and volutrauma.1 Despite improvements in neonatal care, postnatal adverse exposures continue to be important factors in BPD pathogenesis. Emerging evidence also suggests that pulmonary outcomes after preterm birth are likely determined not only by postnatal factors but also by the in utero environment.
Male gender, white race, smoking, hypertension and infection have all been linked to increased BPD susceptibility. In addition, growing evidence suggests that fetal growth restriction (FGR) is a major risk factor for BPD.2 Abnormal placentation resulting in impaired placental perfusion is one of the most frequent causes of early FGR (<32 weeks gestational age) and preeclampsia. In the French EPIPAGE-2 study of preterm infants <32 weeks gestation, the risk of moderate/severe BPD was more than sixfold higher in FGR infants.3 Importantly, FGR has also been linked …
Contributors KY, IS and NC contributed to the drafting and writing of this editorial and approved the final submitted editorial.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.
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