Treat the Symptom, Not the Cause? Pitolisant for Sleepiness in Obstructive Sleep Apnea

phagocytosis (15, 16). In future studies, it will be important to define which IGF-1–dependent cellular functions are modified by rhIGF-1 treatment. Because most preterm infants who develop BPD have been exposed to more than one inciting “injury,” it would be useful to evaluate the efficacy of rhIGF-1 in “multihit” preclinical models of BPD (e.g., antenatal endotoxin followed by postnatal hyperoxia). Finally, because IGF-1 is a potent mitogen (17), longer-term preclinical and human studies are needed to examine its efficacy and safety in neonatal therapy. Nevertheless, the promising findings by Seedorf and colleagues lay the groundwork for future work evaluating rhIGF-1/BP3 as a possible therapeutic strategy for BPD. Of note, a phase 2 RCT (ClinicalTrials.gov Identifier: NCT03253263) evaluating the efficacy of rhIGF-1/BP-3 administration in preterm infants to prevent chronic lung disease through 12 months of corrected age (secondary outcome: BPD at 36 wk) is currently underway. Data from this trial should provide muchneeded evidence regarding the usefulness of rhIGF-1/BP3 as a novel therapy to prevent and/or treat prematurity-associated lung disease. n