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纤维细胞生长因子23在感染性休克和心肌损伤期间在ICU患者中

Zheng Yang¹, Jie Wang¹, Jilin Ma²

¹Department of Intensive Care Unit, Hangzhou Red Cross Hospital, 208 Huancheng Road East, Hangzhou, 310003, Zhejiang, China.

|March 21, 2024

概括

纤维细胞生长因子23 (FGF23) 水平随着炎症和心肌损伤而增加. FGF23在幸存者中正常化,但在非幸存者中没有正常化,这表明它在败血症引起的心脏损伤中的作用.

科学领域:

生物化学生物化学
心脏病学心脏病学
关键护理医学关键护理医学

背景情况:

纤维细胞生长因子23 (FGF23) 是心血管疾病和炎症的已知生物标志物.
败血症可能导致心肌损伤,这是一个严重并发症,死亡率很高.
对于FGF23在败血症相关心肌损伤中的作用仍然不完全理解.

研究的目的:

为了研究血清FGF23水平和心肌损伤在患有败血性休克的患者之间的关联.
评估FGF23与炎症和败血症临床结果相关的动态变化.

主要方法:

血清中FGF23,Klotho,炎症标志物 (CRP,IL-6,WBC) 和心肌损伤标志物 (cTnI,NT-proBNP) 的水平在29名败血症休克患者和29名健康对照中测量.
测量是在败血症休克的高峰期和解决方案后或死亡之前进行的.
分析了FGF23与其他生物标志物之间的相关性,以及临床结果.

主要成果:

与健康对照组相比,败血性休克患者的FGF23水平显着更高 (p < 0.0001).
在幸存者中,峰值FGF23水平高于缓解后水平 (p < 0.0001),与炎症标志物 (CRP,PCT,WBC) 和心肌损伤标志物 (cTnI,NT-proBNP) 有很强的相关性.
在非幸存者中没有观察到FGF23的显著变化,FGF23与Klotho没有相关性.

结论:

升高的FGF23水平与感染性休克期间的炎症和心肌损伤有关.
幸存者的FGF23水平随着炎症的缓解而下降,这表明在败血症中发挥了动态作用.
在性休克患者的心肌损伤的病理生理学中,FGF23可能与之有关.

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