Activation of the Intrinsic Pathway of Coagulation in Children with Meningococcal Septic Shock

Walter A Wuillemin; Karin Fijnvandraat; Bert H F Derkx; Marjolein Peters; Willem Vreede; Hugo ten Cate; C Erik Hack

doi:10.1055/s-0038-1649961

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1995; 74(06): 1436-1441
DOI: 10.1055/s-0038-1649961

Original Articles

Clinical Studies

Schattauer GmbH Stuttgart

Activation of the Intrinsic Pathway of Coagulation in Children with Meningococcal Septic Shock

Authors

Walter A Wuillemin

¹The Central Laboratory of the Netherlands Red Cross Blood Transfusion Service and Laboratory for Clinical and Experimental Immunology, University of Amsterdam, Amsterdam, The Netherlands
Karin Fijnvandraat

²The Emma Kinder Ziekenhuis/Children’s AMC, Amsterdam, The Netherlands
Bert H F Derkx

²The Emma Kinder Ziekenhuis/Children’s AMC, Amsterdam, The Netherlands
Marjolein Peters

²The Emma Kinder Ziekenhuis/Children’s AMC, Amsterdam, The Netherlands
Willem Vreede

³The Pediatric Intensive Care, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Hugo ten Cate

⁴The Center for Hemostasis, Thrombosis, Atherosclerosis, and Inflammation Research, Academic Medical Center, and Slotervaart Ziekenhuis, Department of Internal Medicine, Amsterdam, The Netherlands
C Erik Hack

¹The Central Laboratory of the Netherlands Red Cross Blood Transfusion Service and Laboratory for Clinical and Experimental Immunology, University of Amsterdam, Amsterdam, The Netherlands

⁵The Department of Internal Medicine, Free University Hospital, Amsterdam, The Netherlands

Abstract

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Summary

Meningococcal septic shock (MSS) is complicated by activation of coagulation, fibrinolytic, and complement systems. We studied the contact system of the intrinsic pathway of coagulation in thirteen children with MSS. Activation was assessed upon admittance to the intensive care unit and 48 h thereafter, based on the measurement of factor XII- (FXII), prekallikrein- and factor XI (FXI) antigen levels, as well as on the detection of FXIa-FXIa inhibitor, FXIIa-C1-inhibitor, and kallikrein-C1-inhibitor complexes, respectively. Levels of FXII, prekallikrein and FXI were reduced to about 50% in all patients on admission, and were significantly higher 48 h later. FXIIa-C1-inhibitor complexes were elevated in 7 patients, and kallikrein-C1-inhibitor complexes in 2 patients. FXIa-α₁-antitrypsin complexes were elevated in all patients, FXIa-C1-inhibitor complexes in nine, and FXIa-anti-thrombin III complexes in one patient. We conclude that patients with MSS have activation of the contact system, which may contribute to activation of coagulation, and thus to morbidity and mortality.

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References

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