Yang Wen-Chien, Chen Chien-Yi, Chou Hung-Chieh, Hsieh Wu-Shiun, Tsao Po-Nien
Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan; Department of Pediatrics, National Taiwan University Hospital, Hsin-Chu Branch, Hsinchu, Taiwan.
Department of Pediatrics, National Taiwan University Hospital, Taipei, Taiwan.
Pediatr Neonatol. 2015 Dec;56(6):382-5. doi: 10.1016/j.pedneo.2015.02.001. Epub 2015 Apr 20.
Bronchopulmonary dysplasia (BPD) of prematurity is associated with impaired angiogenesis. Excess soluble fms-like tyrosine kinase-1 (sFlt-1) and lower levels of vascular endothelial growth factor (VEGF) impaired alveolarization in preterm rats. Overexpression of placenta growth factor (PlGF) in mice caused airspace enlargement, which is similar to BPD pathologically. Our study aimed to clarify whether cord blood levels of these angiogenic factors were associated with the development of BPD in preterm infants.
Preterm infants of gestational age (GA) <35 weeks who already had all the data of cord blood VEGF, PlGF, and sFlt-1 levels in our previous studies were enrolled. Cord blood levels of VEGF, PlGF, and sFlt-1 were collected. BPD was defined as the need for supplemental oxygen or mechanical ventilation support at the postmenstrual age of 36 weeks. We used the Mann-Whitney U test for comparison between infants with and without BPD, and multivariate analysis with logistic regression to assess the association of these molecules and the development of BPD.
Infants with BPD had lower GA [(27 weeks (24-34) vs. 31 weeks (28-24)], lower birth body weight [882 g (620-1232) vs. 1538 g (886-2328)], a higher incidence of respiratory distress syndrome (RDS) (58% vs. 14%), and a higher level of PlGF [21.45 pg/dL (6.03-474.01) vs. 7.43 pg/dL (0.09-23.75)] as compared with those infants without BPD. The levels of VEGF and sFlt-1 did not differ significantly between the two groups. Multivariate logistic regression revealed that lower birth body weight (p = 0.022) and higher level of PlGF (p = 0.012) were significantly correlated with the development of BPD independently. There was no significant association between the level of VEGF or sFlt-1 and the development of BPD.
Cord blood level of PlGF, rather than VEGF or sFlt-1, was significantly increased in the BPD group. Consistent with our previous report, cord blood level of PlGF may be considered as a biomarker to predict subsequently developing BPD in preterm infants.
早产相关的支气管肺发育不良（BPD）与血管生成受损有关。过量的可溶性fms样酪氨酸激酶-1（sFlt-1）和较低水平的血管内皮生长因子（VEGF）会损害早产大鼠的肺泡化。小鼠中胎盘生长因子（PlGF）的过表达导致气腔增大，这在病理上与BPD相似。我们的研究旨在阐明这些血管生成因子的脐血水平是否与早产儿BPD的发生有关。
纳入胎龄（GA）<35周且在我们之前的研究中已有脐血VEGF、PlGF和sFlt-1水平所有数据的早产儿。收集脐血VEGF、PlGF和sFlt-1水平。BPD定义为在月经后36周时需要补充氧气或机械通气支持。我们使用Mann-Whitney U检验比较有和无BPD的婴儿，并使用逻辑回归进行多变量分析以评估这些分子与BPD发生之间的关联。
与无BPD的婴儿相比，有BPD的婴儿胎龄更低[（27周（24 - 34）对31周（28 - 34）]，出生体重更低[882 g（620 - 1232）对1538 g（886 - 2328）]，呼吸窘迫综合征（RDS）发生率更高（58%对14%），且PlGF水平更高[21.45 pg/dL（6.03 - 474.01）对7.43 pg/dL（0.09 - 23.75）]。两组间VEGF和sFlt-1水平无显著差异。多变量逻辑回归显示，较低的出生体重（p = 0.022）和较高的PlGF水平（p = 0.012）独立地与BPD的发生显著相关。VEGF或sFlt-1水平与BPD的发生之间无显著关联。
BPD组中PlGF的脐血水平显著升高，而不是VEGF或sFlt-1。与我们之前的报告一致，PlGF的脐血水平可被视为预测早产儿随后发生BPD的生物标志物。
