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

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 tar...
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Autor*in:	Stahl, Klaus [verfasserIn] Schmidt, Julius J. [verfasserIn] Seeliger, Benjamin [verfasserIn] Schmidt, Bernhard M. W. [verfasserIn] Welte, Tobias [verfasserIn] Haller, Hermann [verfasserIn] Hoeper, Marius M. [verfasserIn] Budde, Ulrich [verfasserIn] Bode, Christian [verfasserIn] David, Sascha [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Extracorporeal treatment Septic shock Plasmapheresis ADAMTS-13 von Willebrand factor

Übergeordnetes Werk:	Enthalten in: Critical care - London : BioMed Central, 1997, 24(2020), 1 vom: 02. März
Übergeordnetes Werk:	volume:24 ; year:2020 ; number:1 ; day:02 ; month:03

Links:	Volltext

DOI / URN:	10.1186/s13054-020-2799-5

Katalog-ID:	SPR038972654

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520			\|a 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, R2 = 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.
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allfields	10.1186/s13054-020-2799-5 doi (DE-627)SPR038972654 (SPR)s13054-020-2799-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Stahl, Klaus verfasserin aut Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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, R2 = 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. Extracorporeal treatment (dpeaa)DE-He213 Septic shock (dpeaa)DE-He213 Plasmapheresis (dpeaa)DE-He213 ADAMTS-13 (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Schmidt, Julius J. verfasserin aut Seeliger, Benjamin verfasserin aut Schmidt, Bernhard M. W. verfasserin aut Welte, Tobias verfasserin aut Haller, Hermann verfasserin aut Hoeper, Marius M. verfasserin aut Budde, Ulrich verfasserin aut Bode, Christian verfasserin aut David, Sascha verfasserin aut Enthalten in Critical care London : BioMed Central, 1997 24(2020), 1 vom: 02. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:24 year:2020 number:1 day:02 month:03 https://dx.doi.org/10.1186/s13054-020-2799-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 24 2020 1 02 03
spelling	10.1186/s13054-020-2799-5 doi (DE-627)SPR038972654 (SPR)s13054-020-2799-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Stahl, Klaus verfasserin aut Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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, R2 = 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. Extracorporeal treatment (dpeaa)DE-He213 Septic shock (dpeaa)DE-He213 Plasmapheresis (dpeaa)DE-He213 ADAMTS-13 (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Schmidt, Julius J. verfasserin aut Seeliger, Benjamin verfasserin aut Schmidt, Bernhard M. W. verfasserin aut Welte, Tobias verfasserin aut Haller, Hermann verfasserin aut Hoeper, Marius M. verfasserin aut Budde, Ulrich verfasserin aut Bode, Christian verfasserin aut David, Sascha verfasserin aut Enthalten in Critical care London : BioMed Central, 1997 24(2020), 1 vom: 02. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:24 year:2020 number:1 day:02 month:03 https://dx.doi.org/10.1186/s13054-020-2799-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 24 2020 1 02 03
allfields_unstemmed	10.1186/s13054-020-2799-5 doi (DE-627)SPR038972654 (SPR)s13054-020-2799-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Stahl, Klaus verfasserin aut Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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, R2 = 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. Extracorporeal treatment (dpeaa)DE-He213 Septic shock (dpeaa)DE-He213 Plasmapheresis (dpeaa)DE-He213 ADAMTS-13 (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Schmidt, Julius J. verfasserin aut Seeliger, Benjamin verfasserin aut Schmidt, Bernhard M. W. verfasserin aut Welte, Tobias verfasserin aut Haller, Hermann verfasserin aut Hoeper, Marius M. verfasserin aut Budde, Ulrich verfasserin aut Bode, Christian verfasserin aut David, Sascha verfasserin aut Enthalten in Critical care London : BioMed Central, 1997 24(2020), 1 vom: 02. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:24 year:2020 number:1 day:02 month:03 https://dx.doi.org/10.1186/s13054-020-2799-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 24 2020 1 02 03
allfieldsGer	10.1186/s13054-020-2799-5 doi (DE-627)SPR038972654 (SPR)s13054-020-2799-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Stahl, Klaus verfasserin aut Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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, R2 = 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. Extracorporeal treatment (dpeaa)DE-He213 Septic shock (dpeaa)DE-He213 Plasmapheresis (dpeaa)DE-He213 ADAMTS-13 (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Schmidt, Julius J. verfasserin aut Seeliger, Benjamin verfasserin aut Schmidt, Bernhard M. W. verfasserin aut Welte, Tobias verfasserin aut Haller, Hermann verfasserin aut Hoeper, Marius M. verfasserin aut Budde, Ulrich verfasserin aut Bode, Christian verfasserin aut David, Sascha verfasserin aut Enthalten in Critical care London : BioMed Central, 1997 24(2020), 1 vom: 02. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:24 year:2020 number:1 day:02 month:03 https://dx.doi.org/10.1186/s13054-020-2799-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 24 2020 1 02 03
allfieldsSound	10.1186/s13054-020-2799-5 doi (DE-627)SPR038972654 (SPR)s13054-020-2799-5-e DE-627 ger DE-627 rakwb eng 610 ASE 44.00 bkl Stahl, Klaus verfasserin aut Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier 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, R2 = 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. Extracorporeal treatment (dpeaa)DE-He213 Septic shock (dpeaa)DE-He213 Plasmapheresis (dpeaa)DE-He213 ADAMTS-13 (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213 Schmidt, Julius J. verfasserin aut Seeliger, Benjamin verfasserin aut Schmidt, Bernhard M. W. verfasserin aut Welte, Tobias verfasserin aut Haller, Hermann verfasserin aut Hoeper, Marius M. verfasserin aut Budde, Ulrich verfasserin aut Bode, Christian verfasserin aut David, Sascha verfasserin aut Enthalten in Critical care London : BioMed Central, 1997 24(2020), 1 vom: 02. März (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:24 year:2020 number:1 day:02 month:03 https://dx.doi.org/10.1186/s13054-020-2799-5 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 24 2020 1 02 03
language	English
source	Enthalten in Critical care 24(2020), 1 vom: 02. März volume:24 year:2020 number:1 day:02 month:03
sourceStr	Enthalten in Critical care 24(2020), 1 vom: 02. März volume:24 year:2020 number:1 day:02 month:03
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Extracorporeal treatment Septic shock Plasmapheresis ADAMTS-13 von Willebrand factor
dewey-raw	610
isfreeaccess_bool	true
container_title	Critical care
authorswithroles_txt_mv	Stahl, Klaus @@aut@@ Schmidt, Julius J. @@aut@@ Seeliger, Benjamin @@aut@@ Schmidt, Bernhard M. W. @@aut@@ Welte, Tobias @@aut@@ Haller, Hermann @@aut@@ Hoeper, Marius M. @@aut@@ Budde, Ulrich @@aut@@ Bode, Christian @@aut@@ David, Sascha @@aut@@
publishDateDaySort_date	2020-03-02T00:00:00Z
hierarchy_top_id	331258269
dewey-sort	3610
id	SPR038972654
language_de	englisch
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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, R2 = 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. 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author	Stahl, Klaus
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topic_title	610 ASE 44.00 bkl Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock Extracorporeal treatment (dpeaa)DE-He213 Septic shock (dpeaa)DE-He213 Plasmapheresis (dpeaa)DE-He213 ADAMTS-13 (dpeaa)DE-He213 von Willebrand factor (dpeaa)DE-He213
topic	ddc 610 bkl 44.00 misc Extracorporeal treatment misc Septic shock misc Plasmapheresis misc ADAMTS-13 misc von Willebrand factor
topic_unstemmed	ddc 610 bkl 44.00 misc Extracorporeal treatment misc Septic shock misc Plasmapheresis misc ADAMTS-13 misc von Willebrand factor
topic_browse	ddc 610 bkl 44.00 misc Extracorporeal treatment misc Septic shock misc Plasmapheresis misc ADAMTS-13 misc von Willebrand factor
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title	Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock
ctrlnum	(DE-627)SPR038972654 (SPR)s13054-020-2799-5-e
title_full	Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock
author_sort	Stahl, Klaus
journal	Critical care
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author_browse	Stahl, Klaus Schmidt, Julius J. Seeliger, Benjamin Schmidt, Bernhard M. W. Welte, Tobias Haller, Hermann Hoeper, Marius M. Budde, Ulrich Bode, Christian David, Sascha
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title_sort	effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock
title_auth	Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock
abstract	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, R2 = 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.
abstractGer	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, R2 = 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.
abstract_unstemmed	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, R2 = 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.
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container_issue	1
title_short	Effect of therapeutic plasma exchange on endothelial activation and coagulation-related parameters in septic shock
url	https://dx.doi.org/10.1186/s13054-020-2799-5
remote_bool	true
author2	Schmidt, Julius J. Seeliger, Benjamin Schmidt, Bernhard M. W. Welte, Tobias Haller, Hermann Hoeper, Marius M. Budde, Ulrich Bode, Christian David, Sascha
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