Joung K E, Burris H H, Van Marter L J, McElrath T F, Michael Z, Tabatabai P, Litonjua A A, Weiss S T, Christou H
Goryeb Children's Hospital/Morristown Medical Center, Morristown, NJ, USA.
Harvard Medical School, Boston, MA, USA.
J Perinatol. 2016 Oct;36(10):878-82. doi: 10.1038/jp.2016.115. Epub 2016 Jul 28.
Vitamin D deficiency is associated with asthma and reactive airway disease in childhood but its potential contribution to bronchopulmonary dysplasia (BPD) in preterm infants is unknown. Preterm infants have lower levels of 25-hydroxyvitamin D (25(OH)D) at birth and are at risk for nutritional deficiencies after birth. The objective of the study was to evaluate the association of 25(OH)D concentrations at birth and at 36 weeks' corrected gestational age with BPD in preterm infants born before 29 completed weeks of gestation.
We collected umbilical cord blood samples from 44 preterm infants (gestational age <29 weeks) delivered at Brigham and Women's Hospital in Boston. In addition, with parental consent we collected venous samples at 36 weeks' corrected age from 20 preterm infants born before 29 weeks' gestation (including 6 infants with previously collected cord blood). Samples were frozen at -80 °C until subsequent measurement of 25(OH)D levels by chemiluminescence. We used multivariable logistic models to adjust for gestational age and considered other confounding variables, including maternal race, age, mode of delivery and infant sex.
Among 44 infants, 41 (93.2%) survived and 3 (6.8%) died before 36 weeks' corrected age. Median 25(OH)D levels at birth were 30.4 ng ml(-1) in preterm infants who subsequently died or developed BPD and 33.8 ng ml(-1) in infants who survived without BPD (P=0.6). Median 25(OH)D levels at corrected age of 36 weeks were 59.0 ng ml(-1) among survivors without BPD and 64.2 ng ml(-1) among survivors with BPD (P=0.9). Neither cord blood nor 36 weeks' corrected 25(OH)D levels were associated with odds of death or BPD (adjusted odds ratio (OR) 1.00, 95% confidence interval (CI): 0.73 to 1.37; and OR 0.93, 95% CI: 0.61 to 1.43, respectively).
Among this population of extremely preterm infants neither cord blood nor the 36 weeks' corrected age 25(OH)D levels were associated with development of BPD. Notably, at the current level of supplementation, all extremely preterm infants in our cohort had achieved 25(OH)D levels >30 ng ml(-1) by 36 weeks' corrected age, which is thought to represent sufficiency in adult and pediatric populations.
维生素D缺乏与儿童哮喘及反应性气道疾病相关,但其对早产儿支气管肺发育不良(BPD)的潜在影响尚不清楚。早产儿出生时25-羟维生素D(25(OH)D)水平较低,出生后有营养缺乏风险。本研究的目的是评估妊娠29周前出生的早产儿出生时及矫正胎龄36周时25(OH)D浓度与BPD的关系。
我们从波士顿布里格姆妇女医院分娩的44例早产儿(胎龄<29周)中采集了脐带血样本。此外,在获得家长同意后,我们从20例妊娠29周前出生的早产儿(包括6例之前已采集脐带血的婴儿)矫正年龄36周时采集了静脉样本。样本在-80°C下冷冻,直至随后通过化学发光法测量25(OH)D水平。我们使用多变量逻辑模型对胎龄进行校正,并考虑了其他混杂变量,包括母亲种族、年龄、分娩方式和婴儿性别。
44例婴儿中,41例(93.2%)存活,3例(6.8%)在矫正年龄36周前死亡。随后死亡或发生BPD的早产儿出生时25(OH)D水平中位数为30.4 ng/ml,未发生BPD的存活婴儿为33.8 ng/ml(P = 0.6)。矫正年龄36周时,未发生BPD的存活婴儿25(OH)D水平中位数为59.0 ng/ml,发生BPD的存活婴儿为64.2 ng/ml(P = 0.9)。脐带血及矫正年龄36周时的25(OH)D水平均与死亡或BPD的几率无关(校正优势比(OR)分别为1.00,95%置信区间(CI):0.73至1.37;以及OR 0.93,95%CI:0.61至1.43)。
在这群极早产儿中,脐带血及矫正年龄36周时的25(OH)D水平均与BPD的发生无关。值得注意的是,在目前的补充水平下,我们队列中的所有极早产儿在矫正年龄36周时25(OH)D水平均>30 ng/ml,这被认为在成人和儿童群体中代表充足水平。