What is the basis for a genetic approach in neonatal disorders?

Gene–environment interactions likely account for some degree of the variance in response rates that are clinically observed with antenatal corticosteroids, breast milk prophylaxis, surfactant administration, early recognition and treatment of sepsis, utility of non-invasive ventilation, and judicious exposure to supplemental oxygen. While these therapies and practice guidelines have significantly decreased overall neonatal mortality in the NICU, they have not made a marked impact on the frequency and severity of conditions such as bronchopulmonary dysplasia (BPD), necrotizing enterocolitis, and periventricular leukomalacia. One possible explanation is that genetic factors in the neonate modulate response to external intervention or preventative agents, culminating in variable levels of injury and different degrees of resolution and repair. Gene–environment explanations are supported by the observed heritability of BPD in twin studies, but they do not differentiate the interactions between neonate and offending toxin or pathogen, from interactions between neonate and intervention or therapeutic agent. Likely, both kinds of interactions are important in determining outcome.