短妊娠间隔增加婴儿早期神经发育迟缓风险以及母婴糖代谢紊乱的中介作用

Interpregnancy interval and early infant neurodevelopment: the role of maternal-fetal glucose metabolism

妊娠间隔与婴儿早期神经发育：母婴糖代谢的作用

Authors: Ruirui Ma, Peng Wang，Qiaolan Yang, Yuanyuan Zhu, Lei Zhang, Yuhong Wang, Lijun Sun, Wenxiang Li, Jinfang Ge, Peng Zhu

Source: BMC Med. 2024;22(1):2.

Doi: 10.1186/s12916-023-03191-0

Abstract

Background: Interpregnancy interval (IPI) is associated with a variety of adverse maternal and infant outcomes. However, reports of its associations with early infant neurodevelopment are limited and the mechanisms of this association have not been elucidated. Maternal-fetal glucose metabolism has been shown to be associated with infant neurodevelopmental. The objective of this study was to determine whether this metabolism plays a role in the relationship between IPI and neurodevelopment.

Methods: This prospective birth cohort study included 2599 mother-infant pairs. The IPI was calculated by subtracting the gestational age of the current pregnancy from the interval at the end of the previous pregnancy. Neurodevelopmental outcomes at 12 months in infants were assessed by the Ages and Stages Questionnaire Edition 3 (ASQ-3). Maternal fasting venous blood was collected at 24-28 weeks and cord blood was collected at delivery. The association between IPI and neurodevelopment was determined by logistic regression. Mediation and sensitivity analyses were also conducted.

Results: In our cohort, 14.0% had an IPI <12 months. IPI <12 months increased the failure of the communication domain, fine motor domain, and personal social domain of the ASQ (relative risks (RRs) with 95% confidence interval (CI): 1.73[1.11,2.70]; 1.73[1.10,2.72]; 1.51[1.00,2.29]). Maternal homeostasis model assessment of insulin resistance (HOMA-IR) and cord blood C-peptide was significantly associated with failure in the communication domain [RRs with 95% CI: 1.15(1.02, 1.31); 2.15(1.26, 3.67)]. The proportion of the association between IPI and failure of the communication domain risk mediated by maternal HOMA-IR and cord blood C-peptide was 14.4%.

Conclusions: IPI <12 months was associated with failing the communication domain in infants. Maternal-fetal glucose metabolism abnormality may partially explain the risk of neurodevelopmental delay caused by short IPI.

Keywords: interpregnancy interval, neurodevelopment, glucose, HOMA-IR.

摘要

背景

妊娠间隔（Interpregnancy interval, IPI）与多种不良的母婴结局结局有关。然而，有关其与婴儿早期神经发育相关性的研究报道却很有限，并且这种关联的机制也尚未阐明。母婴糖代谢已被证明与婴儿神经发育有关。本研究旨在确定这种代谢是否在IPI与神经发育之间的关系中发挥作用。

方法

这项前瞻性出生队列研究纳入了2599对母婴。IPI是通过将上一次妊娠结束后至下一次妊娠的时间间隔减去当时的孕周来计算的。用Ages and Stages Questionnaire Edition 3（ASQ-3）对婴儿12个月时的神经发育结果进行评估。孕妇于孕期24-28周采集空腹静脉血样本，而脐带血样本则在分娩时采集。使用 logistic 回归分析了IPI与神经发育之间的关联，同时进行了中介和敏感性分析。

结果

在我们的队列中，有14.0%女性的IPI <12个月，IPI <12个月增加了ASQ中的沟通、精细动作和个人社交能区的发育迟缓风险[相对风险(RR)及95%置信区间（CI）分别为：1.73 (1.11, 2.70); 1.73 (1.10, 2.72); 1.51 (1.00, 2.29)]。母体的胰岛素抵抗稳态模型评估（HOMA-IR）和脐血C肽与婴儿沟通能区的发育迟缓风险显著相关 [RR及95% CI分别为：1.15 (1.02, 1.31); 2.15 (1.26, 3.67)]。由母体 HOMA-IR 和脐血C肽介导的IPI与沟通能区发育迟缓风险之间的关联比例为 14.4%。

结论

IPI小于12个月与婴儿沟通能区发育迟缓有关。母婴糖代谢异常可能部分解释了短IPI引发婴儿神经发育迟缓的风险。