Thromb Haemost 1991; 66(04): 426-429
DOI: 10.1055/s-0038-1646432
Review Article
Schattauer GmbH Stuttgart

Deep Vein Thrombosis and Fibrinolysis

Defective Urokinase Type Plasminogen Activator Release
Marcel Levi
1  The Centre for Thrombosis, Haemostasis and Atherosclerosis Research, Academic Medical Center, Amsterdam, The Netherlands
,
Anthonie W A Lensing
1  The Centre for Thrombosis, Haemostasis and Atherosclerosis Research, Academic Medical Center, Amsterdam, The Netherlands
,
Harry R Büller
1  The Centre for Thrombosis, Haemostasis and Atherosclerosis Research, Academic Medical Center, Amsterdam, The Netherlands
,
Paolo Prandoni
2  The Institute of Internal Medicine, University of Padua, Padua, Italy
,
Gerard Dooijewaard
3  The Gaubius Institute TNO, Leiden, The Netherlands
,
Stefano Cuppini
2  The Institute of Internal Medicine, University of Padua, Padua, Italy
,
Jan Wouter ten Cate
1  The Centre for Thrombosis, Haemostasis and Atherosclerosis Research, Academic Medical Center, Amsterdam, The Netherlands
› Author Affiliations
Further Information

Publication History

Received 21 November 1990

Accepted 09 April 1991

Publication Date:
25 July 2018 (online)

Summary

In the present study 57 consecutive patients with a first episode of venographically proven deep vein thrombosis were investigated to evaluate the release of tissue-type plasminogen activator (t-PA) and of urokinase-type plasminogen activator (u-PA) in response to DDAVP stimulation as well as the resting plasminogen activator inhibitor (PAI) concentration, comparing this to the results obtained in 66 similar patients with a clinical suspicion of thrombosis but with a normal venogram. All assays were performed without knowledge of the patient's status.

Four patients in the deep vein thrombosis-group (7%) had an absent u-PA antigen response upon DDAVP infusion, while a normal response was observed in all control subjects. Patients and controls showed similar increases in t-PA antigen level upon DDAVP. High resting PAI antigen levels were encountered in 5 patients in the deep vein thrombosis-group (9%) and in 6 subjects in the control group (9%).

The results from this controlled study indicate that a defective release of u-PA may occur in patients with deep vein thrombosis and may have pathogenetic significance. Furthermore it is concluded that elevation of PAI levels cannot be considered as a specific risk factor for venous thrombosis.