Poster Session 2
Category: Neonatology
Poster Session 2
Ravi P. Chokshi, MD (he/him/his)
Maternal Fetal Medicine Fellow
Penn State Health
HUMMELSTOWN, Pennsylvania, United States
Allen Kunselman, BS, MA
Senior Instructor
Pennsylvania State University College of Medicine: Penn State College of Medicine
Hershey, Pennsylvania, United States
Kathryn McMullen, MD
Resident Physician
Penn State Health Milton S. Hershey Medical Center
Hershey, Pennsylvania, United States
Noor Banihashem Ahmad, BA
Penn State College of Medicine
Hershey, Pennsylvania, United States
Nayera Guirguis
Penn State Hershey
Penn State Hershey, Pennsylvania, United States
Serdar Ural, MD
Professor of Obstetrics & Gynecology
The Pennsylvania State University College of Medicine
The Pennsylvania State University College of Medicine, Pennsylvania, United States
Shaili Amatya, MBBS
Penn State Hershey Medical Center
Hershey, Pennsylvania, United States
Bronchopulmonary dysplasia (BPD) is the most frequent complication of preterm birth, impacting about 50% of infants born before 28 weeks of gestation. Babies born to mothers with preeclampsia are at greater risk of developing BPD. The suspected cause is a disruption in the Vascular Endothelial Growth Factor (VEGF) signaling pathway, which affects fetal alveolar angiogenesis. Placental angiogenic factors, particularly soluble fms-like tyrosine kinase (sFLT-1), interact with the VEGF pathway, and animal studies have shown that sFLT-1 can cause direct fetal lung injury.
While previous research has measured sFLT-1 levels in maternal and cord blood during preeclampsia, no studies have explored whether this biomarker remains in a newborn’s blood after birth or its potential effects. This project aims to measure sFLT-1 levels in neonatal blood samples and investigate whether higher levels are linked to severe BPD. Plasma samples from extremely preterm newborns (born before 28 weeks of gestation) were collected during their first week of life and analyzed using validated ELISA kits to measure sFLT-1 levels. This pilot study tested 35 patients. The primary outcome was the presence or absence of severe BPD, as defined by the NICHD 2019 criteria. The study was approved by our Institutional Review Board. sFLT-1 was detected in all samples, with levels ranging from 191 to 5375 pg/mL and a median of 943 pg/mL. After adjusting for Fetal Growth Restriction (FGR) and maternal hypertension using binary logistic regression, every 100 pg/mL increase in sFLT-1 was associated with an 8.5% increased odds for severe BPD. However, this finding was not statistically significant (OR=1.085, 95% CI: 0.962–1.223, p-value = 0.18). This pilot study is the first to demonstrate that sFLT-1, a placentally secreted angiogenic factor, is consistently present in the early circulation of extremely preterm newborns. Given its influence on the VEGF signaling pathway, sFLT-1 may have downstream effects on fetal and early neonatal development, warranting further research.
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