PEDIATRICS Vol. 122 No. 3 September 2008, pp. 658-659 (doi:10.1542/10.1542/peds.2008-1599)
COMMENTARY |
Bronchopulmonary Dysplasia: A Genetic Disease
Sections of Pulmonary and Critical Care Medicine, Department of Pediatrics, Pediatric Heart Lung Center, University of Colorado School of Medicine and Children's Hospital, Aurora, Colorado
Abbreviations: BPD, bronchopulmonary dysplasia PDA, patent ductus arteriosus
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Survival of low birth weight infants continues to improve because of marked advances in perinatal care,1 yet significant late pulmonary and neurocognitive impairments persist. Bronchopulmonary dysplasia (BPD), the chronic lung disease that follows premature birth, remains a major clinical problem, occurring in an estimated 10000 to 15000 infants each year in the United States alone. As initially described by Northway et al2 more than 40 years ago, BPD was originally characterized as resulting from severe acute lung injury in modestly premature newborns caused by the adverse effects of hyperoxia, inflammation, mechanical ventilation, and infection. These mechanisms are still recognized as major contributors to the pathogenesis of BPD, along with chorioamnionitis, maternal smoking and drug use, and delivery room management.3,4
Over the past decades, however, changes in care, including antenatal steroid therapy, surfactant use, novel ventilator modalities and strategies, aggressive treatment of patent ductus arteriosus (PDA), and other factors, have altered the nature of BPD. Infants now surviving with BPD have been born at far earlier gestational ages than in the past. The "new BPD" is believed to represent less of the effects of severe lung injury and its repair and more of a disruption or arrest of lung development.5 This is illustrated
Address correspondence to Steven H. Abman, MD, Children's Hospital, Pulmonary Medicine, B395, 13123 E Sixteenth Ave, Aurora, CO 80045. E-mail: steven.abman@uchsc.edu
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