الفهرس 
Respiratory Distress SyndromeOnly 14 pages are availabe for public view
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Abstract
Inflammation plays a central role in respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) in the preterm infant. Although antenatally increased concentrations of cytokines in the blood or amniotic fluid stimulate lung maturation and prevent the postnatal development of RDS, they may also initiate the development of BPD.
Postnatally, both inflammatory cytokines and lipid mediator levels are increased in plasma and tracheal aspirates from preterm infants with RDS, and even more so in infants with BPD
The present study was designed to evaluate the use of cord blood CC16 concentrations to predict the development of respiratory distress syndrome and bronchopulmonary dysplasia in preterm newborn.
The study included 95 preterm neonate ≤ 34 weeks of gestation. They were divided into study and control groups according to whether they develop respiratory distress syndrome and bronchopulmonary dysplasia or not.
All patients were subjected to adequate history taking, full clinical examination, CBC, CRP, ABG, and measurement of cord blood CC16, IL6, SPLA2 concentration at birth.
In our study, patients who developed RDS had significantly lower GA and birth weight compared with those who did not develop RDS.
CC16 was significantly lower in RDS group compared with control group while IL-6 was significantly higher in RDS group compared with control group. No significant difference was found between both groups as regards SPLA2.
Also patients with BPD had significantly lower CC16 and significantly higher IL-6 compared with patients who did not develop BPD.
There was significant positive correlation between CC16 and G.A, B.W and significant negative correlation between IL-6 and G.A, B.W.
Our study also revealed that CC16 at a cutoff point ≤1.6 µg/L showed 100% sensitivity and 91.1% specificity in predicting BPD in preterm newborn.