Bronchopulmonary dysplasia (BPD) remains the most prevalent long-term morbidity of surviving extremely preterm infants and is associated with significant health care utilization in infancy and beyond. Recent advances in neonatal care have resulted in improved survival of extremely low birth weight (ELBW) infants; however, the incidence of BPD has not been substantially impacted by novel interventions in this vulnerable population. The multifactorial cause of BPD requires a multi-pronged approach for prevention and treatment. New approaches in assisted ventilation, optimal nutrition, and pharmacologic interventions are currently being evaluated. The focus of this review is the current state of the evidence for pharmacotherapy in BPD. Promising future approaches in need of further study will also be reviewed.

Background Vitamin D deficiency is associated with asthma and reactive airway disease in childhood but its potential contribution to bronchopulmonary dysplasia (BPD) in preterm infants is unknown. Preterm infants have lower levels of 25-hydroxyvitamin D (25[OH]D) at birth and are at risk for nutritional deficiencies after birth. Objective To evaluate the association of 25(OH) D concentrations at birth and at 36 weeks corrected gestational age with BPD in preterm infants born prior to 29 completed weeks of gestation. Methods We collected umbilical cord blood samples from 44 preterm infants (gestational age <29 weeks) delivered at Brigham and Women's Hospital in Boston. In addition, with parental consent we collected venous samples at 36 weeks corrected age from 20 preterm infants born before 29 weeks gestation (including 6 infants with previously collected cord blood). Samples were frozen at -80°C until subsequent measurement of 25(OH) D levels by chemiluminescence. We used multivariable logistic models to adjust for gestational age and considered other confounding variables including maternal race, age, mode of delivery and infant sex. Results Among 44 infants, 41 (93.2%) survived and 3 (6.8%) died before 36 weeks corrected age. Median 25(OH) D levels at birth were 30.4 ng/ml in preterm infants who subsequently died or developed BPD and 33.8 ng/ml in infants who survived without BPD (p=0.6). Median 25(OH) D levels at corrected age of 36 weeks were 59.0 ng/ml among survivors without BPD and 64.2 ng/ml among survivors with BPD (p=0.9). Neither cord blood nor 36 week corrected 25(OH) D levels were associated with odds of death or BPD (adjusted OR 1.00, 95% CI: 0.73-1.37, OR 0.93, 95% CI: 0.61-1.43 respectively). Conclusion Among this population of extremely preterm infants neither cord blood nor the 36 week corrected age 25(OH) D levels were associated with development of BPD. Notably, at the current level of supplementation, all extremely preterm infants in our cohort had achieved 25(OH) D levels >30 ng/ml by 36 weeks corrected age, which is thought to represent sufficiency in adult and pediatric populations.