Abstract
Objectives. To evaluate the predictive characteristics of KL-6 and CC16 for bronchopulmonary dysplasia (BPD) in preterm infants, either independently or in combination. Study Design. This prospective cohort study was performed from 2011 to 2013 with preterm neonates of gestational age ≤32 weeks and birth weight ≤1500 g. Serum KL-6 and CC16 levels were determined 7 and 14 days after birth. Results. Seventy-three preterm infants were studied. BPD was identified in 24 of these infants. After adjusting for potential confounders, serum KL-6 concentrations were found to be elevated in BPD infants at both time points relative to non-BPD infants, while serum CC16 concentrations were lower at 14 days. At both 7 d and 14 d of life the predictive power of KL-6 levels exceeded that of CC16 (area under receiver operating characteristic curve: at 7 d, 0.91 cf. 0.73, P = 0.02; at 14 d, 0.95 cf. 0.85, P = 0.05). The combination of these markers enhanced the sensitivity further. Conclusions. Serum KL-6 levels higher than 79.26 ng/mL at 14 days postpartum in preterm infants predict the occurrence of BPD. CC16 was less predictive than KL-6 at this time point, but KL-6 and CC16 together enhanced the prediction.
Highlights
Bronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung parenchymal injury, occurring primarily in preterm infants [1]
When KL-6 and CC16 combination was considered, KL-6 and CC16 levels on day 14 had the best predictive characteristics (AUC = 0.974, range 0.82–1.03; P < 0.001; Table 5). In this prospective cohort study, we found that serum KL6 was elevated and CC16 was decreased at postpartum days 7 and 14 in preterm infants who subsequently developed BPD
The concentrations of serum KL-6 seemed to be closely related with the severity of BPD
Summary
Bronchopulmonary dysplasia (BPD) is a syndrome of respiratory distress caused by chronic lung parenchymal injury, occurring primarily in preterm infants [1]. For extremely premature infants born at 25 or 26 weeks’ gestation, dependence on oxygen could mean lung immaturity rather than lung injury, and more direct evidence of lung parenchymal injury upon which to rest a diagnosis of BPD is needed [4]. A means of obtaining a definitive diagnosis of BPD should rely on simple clinical observations, or specific biological markers that grade severity, is generalizable, and is able to predict late pulmonary morbidity and neurodevelopmental outcomes. A specific and objective marker that accurately reflects the severity of lung injury is very much needed
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