≤32周胎龄早产儿显著动脉导管未闭与25-羟基维生素D水平的关系

IF 0.7 4区医学 Q4 PATHOLOGY

Fetal and Pediatric Pathology Pub Date : 2023-08-01 DOI:10.1080/15513815.2023.2178866

Emre Baldan, Erbu Yarci

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引用次数: 0

摘要

前言:我们研究了25-羟基维生素D (25-OHD)水平与早产儿血流动力学显著性动脉导管未闭(hsPDA)发展的关系。方法:胎龄≤32周合并hsPDA的新生儿为研究组(n = 25, 20%)，胎龄≤32周未合并PDA/hsPDA的新生儿为对照组(n = 97, 80%)。结果:研究组GA、出生体重(BW)和25-OHD水平均较低(p = 0.002和p = 0.003)。在调整了GA、体重和呼吸窘迫综合征的影响后，多变量logistic回归分析显示，25-OHD水平低的早产儿发生hsPDA的可能性是25-OHD水平正常早产儿的6.407倍(95% CI: 1.656-24.788, p = 0.007)。25-OHD水平每升高1 ng/mL, hsPDA的发生概率降低(OR: 0.894, 95% CI: 0.816-0.98, p = 0.016)。结论:低25-OHD水平可能与hsPDA的发生有关。

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The Association between Hemodynamically Significant Patent Ductus Arteriosus and 25-Hydroxyvitamin D Levels in Preterm Infants ≤32 Weeks Gestational Age.

Introduction: We investigated the relationship between 25-hydroxyvitamin D (25-OHD) levels and the development of hemodynamically significant patent ductus arteriosus (hsPDA) in preterm infants.

Methods: Newborns having a gestational age (GA) of ≤32 weeks with hsPDA consisted the study group (n = 25, 20%), while newborns ≤32 weeks of GA without PDA/hsPDA were the control group (n = 97, 80%).

Results: The study group had lower GA, birth weight (BW) and 25-OHD levels (p < 0.0001, p = 0.002 and p = 0.003, respectively). After adjusting for the effects of GA, BW and the presence of respiratory distress syndrome, multivariable logistic regression analyses demonstrated that preterm infants with low 25-OHD levels were 6.407 (95% CI: 1.656-24.788, p = 0.007) times more likely to experience hsPDA than preterm infants with normal 25-OHD levels. Every 1 ng/mL increase in 25-OHD levels decreased the probability of hsPDA (OR: 0.894, 95% CI: 0.816-0.98, p = 0.016). Conclusion: Low 25-OHD levels may have a role in the development of hsPDA.

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来源期刊

Fetal and Pediatric Pathology 医学-病理学

CiteScore

3.00

自引率

0.00%

发文量

审稿时长

6-12 weeks

期刊介绍： Fetal and Pediatric Pathology is an established bimonthly international journal that publishes data on diseases of the developing embryo, newborns, children, and adolescents. The journal publishes original and review articles and reportable case reports. The expanded scope of the journal encompasses molecular basis of genetic disorders; molecular basis of diseases that lead to implantation failures; molecular basis of abnormal placentation; placentology and molecular basis of habitual abortion; intrauterine development and molecular basis of embryonic death; pathogenisis and etiologic factors involved in sudden infant death syndrome; the underlying molecular basis, and pathogenesis of diseases that lead to morbidity and mortality in newborns; prenatal, perinatal, and pediatric diseases and molecular basis of diseases of childhood including solid tumors and tumors of the hematopoietic system; and experimental and molecular pathology.