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Coagulation in severe sepsis: a central role for thrombomodulin and activated protein C

Coagulation in severe sepsis: a central role for thrombomodulin and activated protein C
Coagulation in severe sepsis: a central role for thrombomodulin and activated protein C


Objectives: To review the mechanisms that cause coagulation abnormalities in sepsis, focusing on the interaction between the vascular endothelium and the circulating coagulation factors, particularly the role of the protein C pathway and thrombomodulin.

Data Sources/Study Selection : Published research abstracts and review articles on the experimental and clinical investigation of the pathophysiology of disseminated intravascular coagulation in sepsis.

Data Extraction and Synthesis : The data provide increasing evidence that the coagulopathy seen in sepsis is a result of a complex imbalance of pro- and anticoagulant pathways. Whereas previous research has largely studied events in the plasma, it is now apparent that reactions on cell surfaces such as the vascular endothelium are important in the control of the regulatory pathways.

Conclusions: The plasma components of the protein C pathway are down-regulated in sepsis. Decreased thrombomodulin expression may cause defective function of the endothelial component of this pathway in septic patients. Treatments must be designed to overcome any functional defect.
0090-3493
S67-S68
Faust, Saul N.
f97df780-9f9b-418e-b349-7adf63e150c1
Heyderman, Robert S.
cd37d4bb-c0fc-4498-9d41-6dad70179661
Levin, Michael
2be78359-2a08-4885-a83c-4f7a6d1de986
Faust, Saul N.
f97df780-9f9b-418e-b349-7adf63e150c1
Heyderman, Robert S.
cd37d4bb-c0fc-4498-9d41-6dad70179661
Levin, Michael
2be78359-2a08-4885-a83c-4f7a6d1de986

Faust, Saul N., Heyderman, Robert S. and Levin, Michael (2001) Coagulation in severe sepsis: a central role for thrombomodulin and activated protein C. Critical Care Medicine, 29 (7), S67-S68.

Record type: Article

Abstract



Objectives: To review the mechanisms that cause coagulation abnormalities in sepsis, focusing on the interaction between the vascular endothelium and the circulating coagulation factors, particularly the role of the protein C pathway and thrombomodulin.

Data Sources/Study Selection : Published research abstracts and review articles on the experimental and clinical investigation of the pathophysiology of disseminated intravascular coagulation in sepsis.

Data Extraction and Synthesis : The data provide increasing evidence that the coagulopathy seen in sepsis is a result of a complex imbalance of pro- and anticoagulant pathways. Whereas previous research has largely studied events in the plasma, it is now apparent that reactions on cell surfaces such as the vascular endothelium are important in the control of the regulatory pathways.

Conclusions: The plasma components of the protein C pathway are down-regulated in sepsis. Decreased thrombomodulin expression may cause defective function of the endothelial component of this pathway in septic patients. Treatments must be designed to overcome any functional defect.

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More information

Published date: July 2001

Identifiers

Local EPrints ID: 144569
URI: http://eprints.soton.ac.uk/id/eprint/144569
ISSN: 0090-3493
PURE UUID: f4c1bda2-ac29-46b2-8619-d641e760006f
ORCID for Saul N. Faust: ORCID iD orcid.org/0000-0003-3410-7642

Catalogue record

Date deposited: 11 May 2010 15:19
Last modified: 08 Jan 2022 03:04

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Contributors

Author: Saul N. Faust ORCID iD
Author: Robert S. Heyderman
Author: Michael Levin

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