Cord blood KL-6, a specific lung injury marker, correlates with the subsequent development and severity of atypical bronchopulmonary dysplasia

Do Hyun Kim, Han Suk Kim, So Yeon Shim, Jin A. Lee, Chang Won Choi, Ee Kyung Kim, Beyong Il Kim, Jung Hwan Choi

Research output: Contribution to journalArticlepeer-review

13 Scopus citations

Abstract

Background: A considerable number of preterm infants may have been exposed to inflammation in utero and may be born with an inflamed lung. Objectives: To determine the impact of antenatal lung injury and inflammatory response on the pathogenesis of bronchopulmonary dysplasia (BPD) according to its clinical pattern, using KL-6 (as a lung injury marker) and C-reactive protein (CRP) (as a marker of inflammatory response). Methods: In this case-control study, a total of 74 infants (<32 weeks of gestation) including BPD with minimal early lung disease ('atypical'; 21 infants), BPD with significant early lung disease ('classic'; 29 infants) and the non-BPD (24 infants) groups underwent KL-6 and CRP in cord blood determinations. Results: The cord plasma KL-6 levels were significantly higher in the atypical and the total BPD groups than in the non-BPD group (median = 60.9 vs. 34.5 U/ml, p = 0.031; 43.5 vs. 34.5 U/ml, p = 0.02). However, the cord plasma CRP levels were not significantly different among the study groups. The cord plasma KL-6 levels in patients with atypical BPD were significantly higher in infants with moderate or severe BPD than in infants with mild BPD (median = 88.3 vs. 41.5 U/ml, p = 0.041) and were found to be significantly correlated with the duration of oxygen therapy (r = 0.502, p = 0.024). Conclusions: The present study shows that cord plasma KL-6, a specific lung injury marker, is increased and objectively reflects disease severity in atypical BPD.

Original languageEnglish
Pages (from-to)223-229
Number of pages7
JournalNeonatology
Volume93
Issue number4
DOIs
StatePublished - Jun 2008

Keywords

  • Antenatal risk factor
  • C-reactive protein
  • Chronic lung disease
  • Intrauterine inflammatory response
  • Pathogenesis, bronchopulmonary dysplasia

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