Background A dysbalanced coagulation system is part of the pathological host response to infection in sepsis. Activation of pro-coagulant pathways and attenuation of anti-coagulant activity ultimately lead to microvascular stasis and consequent organ failure. No treatment approaches specifically targeting this axis are available. We explored the effects of therapeutic plasma exchange (TPE) on microvascular coagulation dysbalance in septic shock. Methods We conducted a prospective single-center study enrolling 31 patients with early septic shock (onset < 12 h) requiring high doses of norepinephrine (NE > 0.4 μg/kg/min). Clinical and biochemical data, including measurement of protein C; a disintegrin and metalloprotease with a thrombospondin type 1 motif, member 13 (ADAMTS13); and von Willebrand factor antigen (vWF:Ag), were obtained before and after TPE against fresh frozen plasma. Results Antithrombotic acting proteins such as antithrombin-III (ATIII) and protein C were markedly reduced in septic patients, but their activity increased after TPE (ATIII, 51% (41–61) vs. 63% (48–70), p = 0.029; protein C, 47% (38–60) vs. 62% (54–69), p = 0.029). Median ADAMTS13 activity was increased by TPE from 27 (21–42) % before to 47 (38–62) % after TPE ( p < 0.001). In contrast, vWF:Ag was elevated and could be reduced by TPE (353 (206–492) IU/dL vs. 170 (117–232) IU/dL, p < 0.001). Regression analysis yielded a correlation between ADAMTS13 activity and platelet count ( p = 0.001, R 2 = 0.316). Conclusions Septic shock was associated with activation of pro-coagulant pathways and simultaneous depletion of anti-coagulant factors. TPE partially attenuated this dysbalance by removing pro- and by replacing anti-coagulant factors. Trial registration ClinicalTrials.gov, NCT03065751 . Retrospectively registered on 28 February 2017.

中文翻译：

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治疗性血浆置换对感染性休克患者内皮活化和凝血相关参数的影响

背景 不平衡的凝血系统是败血症中宿主对感染的病理反应的一部分。促凝途径的激活和抗凝活性的减弱最终导致微血管淤滞和随之而来的器官衰竭。没有专门针对该轴的治疗方法可用。我们探讨了治疗性血浆置换 (TPE) 对感染性休克患者微血管凝血失衡的影响。方法 我们进行了一项前瞻性单中心研究，招募了 31 名需要高剂量去甲肾上腺素（NE > 0.4 μg/kg/min）的早期感染性休克（发作 < 12 小时）患者。临床和生化数据，包括蛋白 C 的测量；具有血小板反应蛋白 1 型基序的去整合素和金属蛋白酶，成员 13 (ADAMTS13)；和血管性血友病因子抗原 (vWF:Ag)，在针对新鲜冷冻血浆的 TPE 之前和之后获得。结果 脓毒症患者的抗血栓作用蛋白如抗凝血酶 III (ATIII) 和蛋白 C 显着降低，但 TPE 后其活性增加（ATIII，51% (41-61) vs. 63% (48-70)，p = 0.029；蛋白 C，47% (38–60) 与 62% (54–69)，p = 0.029。TPE 将 ADAMTS13 活性的中位数从 TPE 之前的 27 (21–42) % 增加到 TPE 之后的 47 (38–62) % ( p < 0.001)。相比之下，vWF:Ag 升高并可以通过 TPE 降低（353 (206–492) IU/dL vs. 170 (117–232) IU/dL，p < 0.001）。回归分析得出 ADAMTS13 活性与血小板计数之间的相关性（p = 0.001，R 2 = 0.316）。结论 感染性休克与促凝途径的激活和抗凝因子的同时耗竭有关。通过去除促凝因子和替代抗凝因子，TPE 部分减轻了这种失衡。试验注册 ClinicalTrials.gov，NCT03065751。于 2017 年 2 月 28 日追溯登记。