Fetal and neonatal programming is the phenomenon describing deviations from normal developmental patterns. These deviations can increase risks for diseases later in life and are an example of phenotypic plasticity seen throughout nature. For instance, infants born with low birth weight, as a marker of an unfavorable intrauterine environment, are programmed differently and may have an increased risk for multiple diseases in adulthood. These risks include coronary heart disease, increased insulin resistance, hypertension, and imbalances in the immune system. This article discusses mechanisms responsible for fetal and neonatal programming. We also introduce possible changes to current clinical management and practices that reflect the current findings of fetal and neonatal programming.
Infants with bronchopulmonary dysplasia (BPD) are known to have developmental delays, but a direct link between oxygen (O (2)) exposure and brain growth has not been explored. Our objective was to test the hypothesis that the use of O (2) is associated with delays in head growth (DHG) in premature infants with BPD. We conducted a retrospective study on a cohort of infants with BPD (birthweight [BW] < 1500 g, gestational age < 34 weeks). The study population was divided into two groups based on their head circumference (HC) measured at birth. Group 1 represented infants with birth HC > or = 50% for their age on growth chart, and Group 2 represented infants with birth HC < 50% for their age. We recorded HC at hospital discharge and at 6 months of age; and the amount of DHG was calculated (DHG = current age in weeks - the age that matches the 50th percentile for current HC). Regression analysis was conducted to determine the relationship between the duration of O (2) use and DHG in both groups, controlling for BW, discharge weight, gender, and duration of mechanical ventilation (MV). Data were expressed in mean +/- standard error of mean. A total of 137 sequential infants with BPD were studied; of them 65 infants were included in group 1 and 72 infants were included in group 2. The 2 groups did not differ in GA, gender total O (2) days, and total days on MV. At hospital discharge there was no difference between groups in terms of DHG (78% versus 83%, respectively). At 6 months of age, there were more infants in group 2 who had DHG (44% versus 67%, respectively; P < 0.01). In group 1, the amount of DHG correlated only with BW ( P = 0.05). It did not correlate with discharge weight, gender, duration of O (2) use, or duration of MV. In group 2, the amount of DHG correlated only with the duration of O (2) use ( P = 0.04) It did not correlate with BW, discharge weight, gender, or duration of MV. Each 10 days of O (2) use in group 2 was associated with 1.5 +/- 0.1 days of DHG. We concluded that duration of O (2) use is associated with a delay in head growth in infants born with HC < 50th percentile. This study does not clarify whether the use of O (2) is a marker of severity of illness or a contributing factor to DHG in infants with BPD. The mechanisms for this relation require further exploration.
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