Thromb Haemost 2008; 100(01): 38-44
DOI: 10.1160/TH07-11-0659
Blood Coagulation, Fibrinolysis and Cellular Haemostasis
Schattauer GmbH

Absolute risk of venous and arterial thromboembolism in thrombophilic families is not increased by high thrombin-activatable fibrinolysis inhibitor (TAFI) levels

Nienke Folkeringa
1   Division of Haemostasis, Thrombosis and Rheology, Department of Haematology, University Medical Center Groningen, The Netherlands
,
Michiel Coppens
2   Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands
,
Nic J. G. M. veeger
1   Division of Haemostasis, Thrombosis and Rheology, Department of Haematology, University Medical Center Groningen, The Netherlands
,
Victor J. J. Bom
3   Department of Pathology and Laboratory Medicine, University Medical Center Groningen, The Netherlands
,
Saskia Middeldorp
2   Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands
,
Karly Hamulyak
4   Department of Hematology, University Hospital Maastricht, The Netherlands
,
Martin H. Prins
5   Department of Clinical Epidemiology and Medical Technology Assessment, University Hospital Maastricht, The Netherlands
,
Harry R. Büller
2   Department of Vascular Medicine, Academic Medical Center, Amsterdam, The Netherlands
,
Jan van der Meer
1   Division of Haemostasis, Thrombosis and Rheology, Department of Haematology, University Medical Center Groningen, The Netherlands
› Author Affiliations
Financial support: This study was supported by the Dutch Heart Foundation (Grant no: 99.187). The funder had no role in the design and conduct of the study, collection, management, analysis, and interpretation of the data; and preparation, review or approval of the manuscript.
Further Information

Publication History

Received: 05 November 2007

Accepted after major revision: 27 April 2008

Publication Date:
22 November 2017 (online)

Summary

High levels of thrombin-activatable fibrinolysis inhibitor (TAFI) are a supposed risk factor for thrombosis. However, results from previous studies are conflicting. We assessed the absolute risk of venous and arterial thromboembolism in subjects with high TAFI levels (>126 U/dl) versus subjects with normal levels, and the contribution of other concomitant thrombophilic defects. Relatives from four identical cohort studies in families with either deficiencies of antithrombin, protein C or protein S, prothrombin 20210A, high factor VIII levels, or hyperhomocysteinemia were pooled. Probands were excluded. Of 1,940 relatives, 187 had high TAFI levels. Annual incidences of venous thromboembolism were 0.23% in relatives with high TAFI levels versus 0.26% in relatives with normal TAFI levels (adjusted relative risk [RR] 0.8; 95% confidence interval [CI], 0.5–1.3). For arterial thrombosis these were 0.31% versus 0.23% (adjusted RR 1.4; 95% CI, 0.9–2.2). High levels of factor VIII, IX and XI were observed more frequently in relatives with high TAFI levels. Only high factor VIII levels were associated with an increased risk of venous and arterial thrombosis, independently of TAFI levels. None of these concomitant defects showed interaction with high TAFI levels. High TAFI levels were not associated with an increased risk of venous and arterial thromboembolism in thrombophilic families.

 
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