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Published on: August 7, 2017
A Time-Based Analysis of Inflammation in Infants at Risk of Bronchopulmonary Dysplasia
Sandrine Leroy1, Elsa Caumette2, Chandra Waddington3
1EA2415, Montpellier University, Montpellier, France; Mobile Pediatrics Intensive Care Unit, Avicenne hospital, AP-HP, Paris, France.
Insights
Systemic inflammation early in preterm infants predicts bronchopulmonary dysplasia (BPD). This inflammation precedes clinical symptoms, suggesting a critical window for interventions in neonatal intensive care.
Area of Science:
- Neonatology
- Immunology
- Pediatric Respiratory Medicine
Background:
- Bronchopulmonary dysplasia (BPD) is a significant complication in preterm infants.
- The role of early neonatal inflammation in BPD development requires precise delineation.
Purpose of the Study:
- To precisely determine the timing and contribution of systemic inflammation to BPD in preterm infants during the neonatal period.
Main Methods:
- Longitudinal study of blood inflammatory biomarkers (IL-6, IL-8, G-CSF) from birth to 42 days in infants <30 weeks gestation.
- Hierarchical mixed-effects regression models adjusted for infant-specific and time-dependent factors.
Main Results:
- Infants who developed BPD showed increased inflammation post-birth compared to controls.
- Sustained inflammation, particularly IL-8 and G-CSF, predicted BPD and was higher in boys and lower birth weight infants.
- Inflammation preceded clinical BPD signs, increased oxygen needs, and neonatal sepsis or necrotizing enterocolitis.
Conclusions:
- Early systemic inflammation in the neonatal period precedes BPD clinical symptoms.
- Identified a vulnerability window, supporting early, targeted intensive care interventions for BPD prevention.
Objective:
To precisely delineate the timing and contribution of inflammation to bronchopulmonary dysplasia (BPD) in preterm infants during the neonatal period.
Study Design:
Longitudinal study of blood inflammatory biomarkers (interleukin [IL]-6, IL-8, and granulocyte colony-stimulating factor) measured between birth and 42 days of age, at high temporal (daily) resolution, in infants born at or below 30 weeks of gestation. Cytokine predictors of BPD at 36 weeks postmenstrual age were adjusted for infant-specific and time-dependent factors, using hierarchical mixed effects regressions models.
Results:
A total of 1518 data points were obtained in 62 infants (mean gestational age of 27 weeks). Infants who developed BPD later on presented increased inflammation after birth compared with infants without BPD. Inflammation was sustained, with gradual attenuation over 2 weeks (IL-8: OR: 6.5 [95% CI: 1.8-24]; granulocyte colony-stimulating factor: 3.3 [1.5-7.6]) and was higher in boys and in infants of lower birth weight. This inflammation preceded the clinical increased requirement in supplemental oxygen characteristic of BPD, and preceded the peak occurrence of neonatal sepsis or necrotizing enterocolitis.
Conclusions:
Systemic inflammation occurs early in the neonatal period and precedes clinical symptoms in infants with BPD. These data provide a discrete vulnerability window period, supporting a role for targeted intensive care interventions during the early phase of BPD.
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