Morikawa Miki, Inoue Yoshiaki, Sumi Yuka, Kuroda Yoko, Tanaka Hiroshi
Department of Emergency and Critical Care Medicine Juntendo University Urayasu Hospital Urayasu Chiba Japan.
Acute Med Surg. 2014 Jun 26;2(1):13-20. doi: 10.1002/ams2.54. eCollection 2015 Jan.
Sepsis-induced disseminated intravascular coagulopathy is associated with a high mortality rate. The function and deformability of polymorphonuclear leukocytes change in patients with sepsis. The goal of this study was to characterize the changes in polymorphonuclear leukocyte deformability in patients with sepsis-induced disseminated intravascular coagulopathy and to evaluate the relationship between the severity of disseminated intravascular coagulopathy and the deformability of polymorphonuclear leukocytes.
Thirty-five patients with sepsis-induced disseminated intravascular coagulopathy at our department were enrolled in this study. These patients were diagnosed with severe sepsis and an acute disseminated intravascular coagulopathy score ≥ 4. Blood samples were obtained from these patients on days 1, 3, and 7. Polymorphonuclear leukocyte deformability was measured with a microchannel flow analyzer, and polymorphonuclear leukocyte activity, represented as CD11b, was measured by flow cytometry. In contrast, 14 patients who fulfilled with sepsis criteria but without complicated disseminated intravascular coagulopathy were also entered in this study.
In patients with sepsis-induced disseminated intravascular coagulopathy, there was a significant correlation between their Japanese Association for Acute Medicine disseminated intravascular coagulopathy score and polymorphonuclear leukocyte deformability, and CD11b expression. Polymorphonuclear leukocytes became more stiffened and CD11b expression was higher in patients with sepsis-induced disseminated intravascular coagulopathy compared to patients without the condition.
Polymorphonuclear leukocyte deformability correlated with the severity of sepsis-induced disseminated intravascular coagulopathy and the response to treatment.
脓毒症诱导的弥散性血管内凝血与高死亡率相关。脓毒症患者多形核白细胞的功能和可变形性会发生变化。本研究的目的是描述脓毒症诱导的弥散性血管内凝血患者多形核白细胞可变形性的变化,并评估弥散性血管内凝血的严重程度与多形核白细胞可变形性之间的关系。
本研究纳入了我院35例脓毒症诱导的弥散性血管内凝血患者。这些患者被诊断为严重脓毒症且急性弥散性血管内凝血评分≥4分。在第1、3和7天采集这些患者的血样。用微通道流动分析仪测量多形核白细胞的可变形性,并用流式细胞术测量以CD11b表示的多形核白细胞活性。相比之下,14例符合脓毒症标准但无并发弥散性血管内凝血的患者也纳入本研究。
在脓毒症诱导的弥散性血管内凝血患者中,其日本急性医学协会弥散性血管内凝血评分与多形核白细胞可变形性及CD11b表达之间存在显著相关性。与未患该病的患者相比,脓毒症诱导的弥散性血管内凝血患者的多形核白细胞变得更僵硬,且CD11b表达更高。
多形核白细胞可变形性与脓毒症诱导的弥散性血管内凝血的严重程度及对治疗的反应相关。