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Published on: June 24, 2019
Serum eotaxin-1 is increased in extremely-low-birth-weight infants with bronchopulmonary dysplasia or death
Jegen Kandasamy1, Claire Roane1, Alexander Szalai2
1Department of Pediatrics, University of Alabama at Birmingham, Birmingham, Alabama.
Insights
Early inflammation in extremely-low-birth-weight (ELBW) infants increases bronchopulmonary dysplasia (BPD) risk. Eotaxin on day 1 helps predict BPD or death in ELBW infants.
Area of Science:
- Neonatal Medicine
- Pediatric Pulmonology
- Biomarker Discovery
Background:
- Systemic inflammation in extremely-low-birth-weight (ELBW) infants is linked to higher bronchopulmonary dysplasia (BPD) rates.
- Identifying early predictors of BPD and mortality in ELBW infants is crucial for timely intervention.
Purpose of the Study:
- To identify circulating biomarkers for predicting BPD or death in ELBW infants.
- To develop predictive models for BPD/death using early postnatal biomarkers and clinical data.
Main Methods:
- Analyzed blood samples from 152 ELBW infants on postnatal day 1 for C-reactive protein (CRP) and 39 cytokines/chemokines.
- Employed forward stepwise regression and Classification and Regression Tree (CART) analysis using CRP, cytokines, and early clinical variables to identify BPD/death predictors.
Main Results:
- Birth weight and eotaxin (CCL11) were significant predictors identified by regression analysis.
- CART analysis revealed FiO2 at 24 hours and eotaxin levels in infants with FiO2 > 28% as key indicators for BPD/death risk.
Conclusions:
- Eotaxin measured on the day of birth is a valuable biomarker for identifying ELBW infants at risk of BPD or death.
- Further research is needed to elucidate eotaxin's role in lung injury and BPD pathogenesis.
Background:
Early systemic inflammation in extremely-low-birth-weight (ELBW) infants is associated with an increased risk of bronchopulmonary dysplasia (BPD). Our objective was to identify circulating biomarkers and develop prediction models for BPD/death soon after birth.
Methods:
Blood samples from postnatal day 1 were analyzed for C-reactive protein (CRP) by enzyme-linked immunosorbent assay and for 39 cytokines/chemokines by a multiplex assay in 152 ELBW infants. The primary outcome was physiologic BPD or death by 36 wk. CRP, cytokines, and clinical variables available at ≤24 h were used for forward stepwise regression and Classification and Regression Tree (CART) analysis to identify predictors of BPD/death.
Results:
Overall, 24% developed BPD and 35% died or developed BPD. Regression analysis identified birth weight and eotaxin (CCL11) as the two most significant variables. CART identified FiO2 at 24 h (11% BPD/death if FiO2 ≤28%, 49% if >28%) and eotaxin in infants with FiO2 > 28% (29% BPD/death if eotaxin was ≤84 pg/ml; 65% if >84) as variables most associated with outcome.
Conclusion:
Eotaxin measured on the day of birth is useful for identifying ELBW infants at risk of BPD/death. Further investigation is required to determine if eotaxin is involved in lung injury and pathogenesis of BPD.
