Yu Yanjuan, Su Yanyan, Jin Xiuhong, Zhang Xiangfeng, Yang Yeran, Shen Yuelin
Respiratory Department, Children's Hospital Affiliated to Zhengzhou University, Henan Children's Hospital, Zhengzhou Children's Hospital, Zhengzhou, 450018, China.
Beijing Key Laboratory for Pediatric Diseases of Otolaryngology, Head and Neck Surgery, MOE Key Laboratory of Major Diseases in Children, Beijing Children's Hospital, Beijing Pediatric Research Institute, Capital Medical University, National Center for Children's Health, NO.56, Nanlishi Road, Beijing, 100045, China.
Ital J Pediatr. 2025 Aug 5;51(1):247. doi: 10.1186/s13052-025-02105-5.
This study aim to investigate the role of endothelial damage in the pathogenesis of Mycoplasma pneumoniae pneumonia (MPP) by comparing serum levels of endothelial cell-specific molecule 1 (ESM-1) and Syndecan-1 in patients with varying degrees of MPP severity. Additionally, we aim to explore the relationship between the production of ESM-1 and Syndecan-1 and the severity of MPP, inflammation, as well as hypercoagulative state in children.
A prospective, observational study that included clinical manifestations, laboratory tests, and serum ESM-1 and Syndecan-1 assays. The correlation between ESM-1 and Syndecan-1 levels with inflammatory markers and coagulation markers was analyzed. Multivariate logistic regression analysis was conducted to identify significant risk factors for Severe Mycoplasma pneumoniae pneumonia (SMPP).
A total of 179 children with MPP and 40 healthy volunteers were enrolled. Serum ESM-1 and Syndecan-1 levels were significantly elevated in children with MPP compared to the healthy children (all P < 0.05). A multivariate analysis revealed that ESM-1, Syndecan-1, D-dimer and LDH were the significant predictors of SMPP, with odds ratios of 1.034, 1.002, 5.042 and 1.014, respectively. The optimal cutoff values of ESM-1, Syndecan-1, D-dimer and LDH for predicting SMPP were 79.67 ng/mL, 3219.35 pg/mL, 0.67 µg/mL and 365.00 U/L, respectively.
ESM-1, Syndecan-1, D-dimer, and LDH can serve as independent predictors for SMPP. The interaction between endothelial damage, excessive inflammatory response, and hypercoagulable state collectively contributes to the development and progression of SMPP.
本研究旨在通过比较不同严重程度的支原体肺炎（MPP）患者血清中内皮细胞特异性分子1（ESM-1）和Syndecan-1的水平，探讨内皮损伤在MPP发病机制中的作用。此外，我们旨在探讨儿童ESM-1和Syndecan-1的产生与MPP严重程度、炎症以及高凝状态之间的关系。
一项前瞻性观察性研究，包括临床表现、实验室检查以及血清ESM-1和Syndecan-1检测。分析了ESM-1和Syndecan-1水平与炎症标志物和凝血标志物之间的相关性。进行多因素逻辑回归分析以确定重症支原体肺炎（SMPP）的重要危险因素。
共纳入179例MPP患儿和40名健康志愿者。与健康儿童相比，MPP患儿血清ESM-1和Syndecan-1水平显著升高（均P < 0.05）。多因素分析显示，ESM-1、Syndecan-1、D-二聚体和乳酸脱氢酶（LDH）是SMPP的重要预测指标，其比值比分别为1.034、1.002、5.042和1.014。预测SMPP的ESM-1、Syndecan-1、D-二聚体和LDH的最佳截断值分别为79.67 ng/mL、3219.35 pg/mL、0.67 μg/mL和365.00 U/L。
ESM-1、Syndecan-1、D-二聚体和LDH可作为SMPP的独立预测指标。内皮损伤、过度炎症反应和高凝状态之间的相互作用共同促进了SMPP的发生和发展。
