EC Paediatrics

Background: Inflammation is central to premature baby respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD). IL6 is a widely distributed collection of enzymes that are principally involved in the turnover of membrane phospholipids and lipid digestion. They are also important for the inflammation pathways because they are the first step in the production of eicosanoids and other inflammatory mediators. It has a dual role because it contributes to the inflammation route and is also the key enzyme engaged in surfactant degradation. To investigate the effect of IL-6 concentration as a predictor of the development of respiratory distress (RDs) and bronchopulmonary dysplasia (BPD) in premature infants.

Methods: The research was carried out at Ain Shams University's Obstetrics and Gynecology Hospital's Labor and Delivery ward and NICU from 12 January 2012 to 28 June 2013. The study involved 95 premature newborns born at less than 34 weeks of gestation. They were split into two groups based on whether they suffered from respiratory distress or not.

The study excluded preterm infants with substantial congenital malformations, inborn errors of metabolism, chromosomal abnormalities, and risk factors for neonatal sepsis, such as premature rupture of membranes, Maternal UTI, Chorioamnionitis, and Rh hemolytic illness.

All patients had a full history taken. On admission, a full clinical examination and laboratory investigations were performed. Blood samples were drawn from the maternal side of the cut end of the umbilical cord for the measurement of serum interleukin 6 (IL-6) levels, radiological investigations, and neonatal follow-up until discharge.

Results: RDS and BPD infants had significantly greater IL-6 concentrations than preterm controls (P < 0.05 and p < 0.01, respectively).

Conclusion: High levels of IL6 in preterm newborn cord blood independently predict the development of RDS and BPD.

 Keywords: Interleukin 6; Respiratory Distress Syndrome; Bronchopulmonary Dysplasia; Preterm Infant; Cord Blood

1. Moodley YP., et al. “Fibroblasts isolated from normal lungs and those with idiopathic pulmonary fibrosis differ in interleukin-6/gp130-mediated cell signaling and proliferation”. The American Journal of Pathology1 (2003): 345-354.
2. Ferreira PJ., et al. “Circulating neutrophil concentration and respiratory distress in premature infants”. The Journal of Pediatrics455 (2000): 72.
3. Rincon M and Irvin CG. “Role of IL-6 in asthma and other inflammatory pulmonary diseases”. International Journal of Biological Sciences 8 (2012): 1281-1290.
4. Jobe AH. “Antenatal factors and the development of bronchopulmonary dysplasia”. Seminars in Fetal and Neonatal Medicine 8 (2003): 9-17.
5. Kramer BW., et al. “Prenatal inflammation and lung development”. Seminars in Fetal and Neonatal Medicine 14 (2009): 2e7.
6. Bancalari E., et al. “Management of bronchopulmonary dysplasia”. In: Maalouf E (edition). Best Practice Guideline, Early Human Development. Oxford: Elsevier (2005).
7. Bhandari A and Bhandari V. “Pitfalls, problems, and progress in bronchopulmonary dysplasia”. Paediatrics123 (2009): 1562-1573.
8. Gomez R., et al. “The fetal inflammatory response syndrome”. American Journal of Obstetrics and Gynecology 179 (1998): 194-202.
9. Yoon BH., et al. “A systemic fetal inflammatory response and the development of bronchopulmonary dysplasia”. American Journal of Obstetrics and Gynecology4 (1999): 773-779.