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Thromb Haemost 1992; 67(06): 623-626
DOI: 10.1055/s-0038-1648512
Original Articles
Schattauer GmbH Stuttgart

Tumor Necrosis Factor Induces von Willebrand Factor Release in Healthy Humans

Tom van der Poll
1   The Department of Internal Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
2   Centre for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
,
Sander J H van Deventer
1   The Department of Internal Medicine, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
2   Centre for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
,
Gerard Pasterkamp
3   Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands
,
Jan A van Mourik
3   Central Laboratory of the Netherlands Red Cross Blood Transfusion Service, Amsterdam, The Netherlands
,
Harry R Büller
2   Centre for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
,
Jan W ten Cate
2   Centre for Haemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

Received 10 June 1991

Accepted after revision 15 January 1992

Publication Date:
03 July 2018 (online)

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Summary

Tumor necrosis factor (TNF) is an important mediator of the host responses to systemic infection. To investigate the effect of TNF on the release of von Willebrand factor (vWF) into the circulation, we performed a controlled study in six healthy men, sequentially measuring the plasma concentrations of vWF antigen after a bolus intravenous injection of recombinant human TNF (50 μg/m2). TNF induced a marked increase in vWF antigen plasma levels, becoming significant after 45 min and peaking after 4 h (percentage increase from base line: 351 ±46; p <0.0001, TNF versus saline). The multimeric organization of circulating vWF was not affected by TNF. We conclude that TNF may be an early mediator of increased vWF secretion in systemic infection.

 

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