Indomethicin and BPD

Abstract

The outcome of bronchopulmonary dysplasia (BPD) in very low birth weight infants (VLBW) has many clinical associations. However, treatments to avoid or decrease adverse effects of those associations have not consistently decreased BPD. For example, antenatal corticosteroids or surfactant treatments to decrease RDS have not decreased the incidence of BPD, although each therapy has decreased mortality and has decreased the severity of BPD. The presumed explanation for the lack of effect on incidence of BPD is that increased survival has put more marginal infants at risk of developing BPD. Similarly, different ventilation strategies have not consistently decreased BPD. BPD is thought to result from injury resulting in lung inflammation, and anti-inflammatory corticosteroids have been used to treat BPD. A patent ductus arteriosis (PDA) also is linked to BPD. However, the cyclo-oxygenase inhibitors, which close the PDA and are anti-inflammatory, have not decreased PDA.Schmidt et al have revisited the Trial of Indomethacin Prophylaxis in Preterms (TIPP) database to demonstrate that randomization of infants to indomethacin may increase BPD because of decreased weight loss and increased supplemental oxygen need. In a very thoughtful editorial, Carl Bose reflects on what other mechanisms might explain why indomethacin does not decrease (and may increase) BPD. The clinical associations with BPD may primarily indicate the immaturity of the infant at risk, and BPD seems to result from interference in the development of the immature lung.Effective therapies to decrease BPD may need to be directed at the abnormal development rather than other associations with immaturity. The outcome of bronchopulmonary dysplasia (BPD) in very low birth weight infants (VLBW) has many clinical associations. However, treatments to avoid or decrease adverse effects of those associations have not consistently decreased BPD. For example, antenatal corticosteroids or surfactant treatments to decrease RDS have not decreased the incidence of BPD, although each therapy has decreased mortality and has decreased the severity of BPD. The presumed explanation for the lack of effect on incidence of BPD is that increased survival has put more marginal infants at risk of developing BPD. Similarly, different ventilation strategies have not consistently decreased BPD. BPD is thought to result from injury resulting in lung inflammation, and anti-inflammatory corticosteroids have been used to treat BPD. A patent ductus arteriosis (PDA) also is linked to BPD. However, the cyclo-oxygenase inhibitors, which close the PDA and are anti-inflammatory, have not decreased PDA. Schmidt et al have revisited the Trial of Indomethacin Prophylaxis in Preterms (TIPP) database to demonstrate that randomization of infants to indomethacin may increase BPD because of decreased weight loss and increased supplemental oxygen need. In a very thoughtful editorial, Carl Bose reflects on what other mechanisms might explain why indomethacin does not decrease (and may increase) BPD. The clinical associations with BPD may primarily indicate the immaturity of the infant at risk, and BPD seems to result from interference in the development of the immature lung. Effective therapies to decrease BPD may need to be directed at the abnormal development rather than other associations with immaturity.