Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock

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...

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Published in:Critical care (London, England) England), 2020-03, Vol.24 (1), p.71-71, Article 71
Main Authors: Stahl, Klaus, Schmidt, Julius J, Seeliger, Benjamin, Schmidt, Bernhard M W, Welte, Tobias, Haller, Hermann, Hoeper, Marius M, Budde, Ulrich, Bode, Christian, David, Sascha
Format: Article
Language:English
Subjects:
ADAMTS-13
Anticoagulants
Antigens
Apheresis
Biochemistry
Care and treatment
Catheters
Coagulation
Critical care
Endothelium
Extracorporeal treatment
Health aspects
Hemodialysis
Infection
Medical research
Methods
Mortality
Pathogens
Patient outcomes
Physiological aspects
Plasma exchange (Therapeutics)
Plasmapheresis
Protein C
Proteins
Regression analysis
Sepsis
Septic shock
Vascular endothelium
Von Willebrand factor
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Summary: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. We conducted a prospective single-center study enrolling 31 patients with early septic shock (onset  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. 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 
ISSN:1364-8535
1466-609X
1364-8535
1366-609X
DOI:10.1186/s13054-020-2799-5