The importance of intra-amniotic inflammation in the subsequent development of atypical chronic lung disease

Joonho Lee, Kyung Joon Oh, Hye Jin Yang, Joong Shin Park, Roberto Romero, Bo Hyun Yoon

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Objective. To examine whether the intra-amniotic inflammation is a risk factor for the development of atypical chronic lung disease CLD. Study design. A retrospective cohort study was undertaken in 72 patients who delivered preterm neonates gestational age: 24-32 weeks within 5 days of amniocentesis and whose neonates subsequently developed CLD. Atypical CLD was defined as CLD without respiratory distress syndrome RDS. Intra-amniotic inflammation was defined as an elevated amniotic fluid AF concentration of matrix metalloproteinase-8 MMP-8 >23 ngml. Results. 1 Atypical CLD was identified in 54.2 3972 of cases with CLD; 2 there were no significant differences in the median gestational age at birth and the rate of antenatal corticosteroid use between infants with atypical CLD and CLD with RDS; 3 preterm newborns with atypical CLD had a significantly higher median AF MMP-8 concentration median 373.1 ngml vs. 8.6 ngml, p 0.003 and median AF white blood cell count median 450.0mm3vs. 5.5mm 3, p 0.009, and a higher rate of intra-amniotic inflammation 74.4vs. 45.5, p 0.012 than those with CLD with RDS. Conclusion. Intra-amniotic inflammation confers a greater risk for atypical CLD than for typical CLD with initial RDS. This novel observation strengthens the importance of prenatal inflammation as a mechanism of lung injury.

Original languageEnglish
Pages (from-to)917-923
Number of pages7
JournalJournal of Maternal-Fetal and Neonatal Medicine
Volume22
Issue number10
DOIs
Publication statusPublished - 2009

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Obstetrics and Gynaecology

Fingerprint Dive into the research topics of 'The importance of intra-amniotic inflammation in the subsequent development of atypical chronic lung disease'. Together they form a unique fingerprint.

Cite this