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2017 年至 2020 年间,在一家单中心对 42 例脓毒症性心肌功能障碍患者的白细胞介素 8 血浆水平进行回顾性观察研究。

A Retrospective Observational Study of the Association Between Plasma Levels of Interleukin 8 in 42 Patients with Sepsis-Induced Myocardial Dysfunction at a Single Center Between 2017 and 2020.

机构信息

Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China (mainland).

Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China (mainland).

出版信息

Med Sci Monit. 2021 Dec 1;27:e933065. doi: 10.12659/MSM.933065.

DOI:10.12659/MSM.933065
PMID:34897267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8647454/
Abstract

BACKGROUND This retrospective, observational study from a single center aimed to evaluate the association between complement (C)3 and C4, lymphocytes markers CD4 and CD8, and the interleukins IL-1ß, IL-2R, IL-6, IL-10, and IL-8 in patients with sepsis-induced myocardial dysfunction (SIMD) and a reduced left ventricular ejection fraction (LVEF) of < 50%. MATERIAL AND METHODS Patients with sepsis from July 2017 to December 2020 were divided into a SIMD group (42 patients) and NO-SIMD group (214 patients). Diagnostic criteria of sepsis were based on SEPSIS 3.0 guidelines. SIMD was defined as LVEF.

摘要

背景

本回顾性观察性研究来自单一中心,旨在评估补体(C)3 和 C4、淋巴细胞标志物 CD4 和 CD8,以及白细胞介素 IL-1β、IL-2R、IL-6、IL-10 和 IL-8 在合并脓毒症性心肌功能障碍(SIMD)和左心室射血分数(LVEF)<50%降低的患者中的相关性。

材料和方法

2017 年 7 月至 2020 年 12 月,将脓毒症患者分为 SIMD 组(42 例)和非 SIMD 组(214 例)。脓毒症的诊断标准基于 SEPSIS 3.0 指南。SIMD 定义为 LVEF。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e2/8647454/cc885a442c6e/medscimonit-27-e933065-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e2/8647454/6b5a8137bc2f/medscimonit-27-e933065-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e2/8647454/cc885a442c6e/medscimonit-27-e933065-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e2/8647454/6b5a8137bc2f/medscimonit-27-e933065-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e2/8647454/cc885a442c6e/medscimonit-27-e933065-g002.jpg

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本文引用的文献

1
Septic Cardiomyopathy: From Basics to Management Choices.脓毒症性心肌病:从基础到治疗选择。
Curr Probl Cardiol. 2021 Apr;46(4):100767. doi: 10.1016/j.cpcardiol.2020.100767. Epub 2020 Dec 11.
2
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J Zhejiang Univ Sci B. 2020 Jul;21(7):537-548. doi: 10.1631/jzus.B2000049.
3
New strategies for treatment of infectious sepsis.治疗感染性败血症的新策略。
Lipid oxidation dysregulation: an emerging player in the pathophysiology of sepsis.
脂质氧化失调:脓毒症病理生理学中的一个新兴参与者。
Front Immunol. 2023 Aug 3;14:1224335. doi: 10.3389/fimmu.2023.1224335. eCollection 2023.
4
Septic Cardiomyopathy: From Pathophysiology to the Clinical Setting.脓毒症性心肌病:从病理生理学到临床环境。
Cells. 2022 Sep 11;11(18):2833. doi: 10.3390/cells11182833.
5
The Relationship between Serum CXCL8 and ET-1 Expression Levels and Sepsis Complicated with Heart Failure.血清CXCL8与ET-1表达水平及脓毒症合并心力衰竭的关系
Cardiol Res Pract. 2022 Aug 27;2022:8570486. doi: 10.1155/2022/8570486. eCollection 2022.
6
The Effect of Sepsis on Myocardial Function: A Review of Pathophysiology, Diagnostic Criteria, and Treatment.脓毒症对心肌功能的影响:病理生理学、诊断标准及治疗的综述
Cureus. 2022 Jun 21;14(6):e26178. doi: 10.7759/cureus.26178. eCollection 2022 Jun.
J Leukoc Biol. 2019 Jul;106(1):187-192. doi: 10.1002/JLB.4MIR1118-425R. Epub 2019 Mar 1.
4
Troponin Testing for Assessing Sepsis-Induced Myocardial Dysfunction in Patients with Septic Shock.肌钙蛋白检测在评估感染性休克患者脓毒症诱导的心肌功能障碍中的应用
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5
Association of IL-8 With Infarct Size and Clinical Outcomes in Patients With STEMI.白细胞介素-8 与 STEMI 患者梗死面积和临床结局的关系。
J Am Coll Cardiol. 2018 Jul 10;72(2):187-198. doi: 10.1016/j.jacc.2018.04.053.
6
Role of complement C5a and histones in septic cardiomyopathy.补体 C5a 和组蛋白在脓毒症性心肌病中的作用。
Mol Immunol. 2018 Oct;102:32-41. doi: 10.1016/j.molimm.2018.06.006. Epub 2018 Jun 18.
7
Pathophysiology, echocardiographic evaluation, biomarker findings, and prognostic implications of septic cardiomyopathy: a review of the literature.脓毒症性心肌病的病理生理学、超声心动图评估、生物标志物研究结果及预后意义:文献复习。
Crit Care. 2018 May 4;22(1):112. doi: 10.1186/s13054-018-2043-8.
8
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Medicine (Baltimore). 2018 Mar;97(13):e0263. doi: 10.1097/MD.0000000000010263.
9
Septic Cardiomyopathy.感染性心肌病。
Crit Care Med. 2018 Apr;46(4):625-634. doi: 10.1097/CCM.0000000000002851.
10
Immune Activation in Sepsis.脓毒症中的免疫激活。
Crit Care Clin. 2018 Jan;34(1):29-42. doi: 10.1016/j.ccc.2017.08.002. Epub 2017 Oct 12.