ronchopulmonary dysplasia (BPD) is the most common morbidity of preterm birth affecting 50% of infants born less than 30 weeks' gestation in the US. 1 Despite preventive efforts, the incidence of BPD is increasing owing to the improved survival of infants born extremely preterm. 2 Recent studies suggest racial disparities may adversely affect outcomes for preterm infants experiencing common neonatal morbidities, including respiratory distress syndrome, intraventricular hemorrhage, and necrotizing enterocolitis, during the initial neonatal intensive care unit (NICU) hospitalization. [3][4][5] However, our knowledge of the association of racial disparities with outcomes for preterm infants with BPD remains unclear.Multiple prospective cohort studies have determined that Black maternal race is independently associated with a de-creased risk of severe BPD at 36 weeks' postmenstrual age (PMA), when the diagnosis of BPD is made. 6,7 Additional analyses of these cohorts, however, also identify Black maternal race as an independent risk factor for increased respiratory morbidity in early childhood. 6,8,9 The mechanisms underlying the finding that preterm infants born to Black mothers are at decreased risk of developing severe BPD but are nonetheless at increased risk of early childhood respiratory morbidity remain unknown.The 2001 National Institutes of Health (NIH) consensus criteria define severe BPD in infants born less than 32 weeks' gestation as the need for supplemental oxygen for 28 days or more and a fraction of inspired oxygen greater than 0.3 and/or positive pressure at 36 weeks' PMA. 10 Short-and long-term outcomes for patients with BPD are highly variable. In this study, IMPORTANCE Bronchopulmonary dysplasia (BPD) is the most common serious morbidity of preterm birth. Short-term respiratory outcomes for infants with the most severe forms of BPD are highly variable. The mechanisms that explain this variability remain unknown and may be mediated by racial disparities.OBJECTIVE To determine the association of maternal race with death and length of hospital stay in a multicenter cohort of infants with severe BPD.
Pulmonary hypertension (PH) and right ventricular hypertrophy (RVH) affect 25-35% of premature infants with significant bronchopulmonary dysplasia (BPD), increasing morbidity and mortality. We sought to determine the role of phosphodiesterase 5 (PDE5) in the right ventricle (RV) and left ventricle (LV) in a hyperoxia-induced neonatal mouse model of PH and RVH. After birth, C57BL/6 mice were placed in room air (RA) or 75% O2 (CH) for 14 days to induce PH and RVH. Mice were euthanized at 14 days or recovered in RA for 14 days or 42 days prior to euthanasia at 28 or 56 days of age. Some pups received sildenafil or vehicle (3 mg·kg(-1)·dose(-1) sc) every other day from P0. RVH was assessed by Fulton's index [RV wt/(LV + septum) wt]. PDE5 protein expression was analyzed via Western blot, PDE5 activity was measured by commercially available assay, and cGMP was measured by enzyme-linked immunoassay. Hyperoxia induced RVH in mice after 14 days, and RVH did not resolve until 56 days of age. Hyperoxia increased PDE5 expression and activity in RV, but not LV + S, after 14 days. PDE5 expression normalized by 28 days of age, but PDE5 activity did not normalize until 56 days of age. Sildenafil given during hyperoxia prevented RVH, decreased RV PDE5 activity, and increased RV cGMP levels. Mice with cardiac-specific overexpression of PDE5 had increased RVH in RA. These findings suggest normal RV PDE5 function is disrupted by hyperoxia, and elevated PDE5 contributes to RVH and remodeling. Therefore, in addition to impacting the pulmonary vasculature, sildenafil also targets PDE5 in the neonatal mouse RV and decreases RVH.
To estimate the association between lung hyperin ation and the time to successful transition to outpatient ventilators in infants with sBPD and chronic respiratory failure. Design/Methods:Infants with sBPD < 32 weeks' gestation who received tracheostomies were identi ed. Hyperin ation was the main exposure. Time from tracheostomy to successful transition to the outpatient device was the main outcome. Kaplan-Meier and multivariable Cox proportional hazards were used to estimate the relationships between hyperin ation and the main outcome. ResultsSixty-two infants were included; 26 (42%) were hyperin ated. Eleven died before transition, and 51 successfully transitioned. Hyperin ation was associated with both mortality (31% vs 8.3%, p = 0.02) and an increased duration (72 vs. 56 days) to successful transition (hazard ratio (HR) = 0.38, 95% CI: 0.19, 0.76, p = 0.006). Growth velocity was similar after tracheostomy placement. ConclusionsIn infants with chronic respiratory failure and sBPD < 32 weeks' gestation, hyperin ation is related to mortality and inpatient morbidities.
Nutrition complications are common in survivors of congenital diaphragmatic hernia (CDH). Infants diagnosed with CDH may demonstrate poor growth despite receiving enteral tube feedings and gastroesophageal reflux treatment. This literature review was conducted to determine nutrition interventions resulting in favorable growth, which may improve outcomes in these infants. Results indicate that early nutrition support, including supplemental parenteral nutrition with provisions of ≥125 kcal/kg/d and ≥2.3 g/kg/d protein (which are higher than dietary reference intakes for infants), may have a positive impact on growth, potentially impacting neurological development.
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