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Table of Contents
Vol. 33, No. 4, 2003
Issue release date: July – August
Section title: Original Paper
Pathophysiol Haemost Thromb 2003;33:192–196

Acquired and Inherited Thrombophilic Factors and the Risk for Residual Venous Thrombosis

Bank I.a · Tick L.W.c · Hutten B.A.b · Kramer M.H.H.c · Middeldorp S.a · Büller H.R.a
Departments of aVascular Medicine and bClinical Epidemiology and Biostatistics, Academic Medical Center, University of Amsterdam, Amsterdam and cDepartment of Internal Medicine, Eemland Hospital, Amersfoort, The Netherlands
email Corresponding Author

I. Bank

Department of Vascular Medicine, Academic Medical Center

F4-277, Meibergdreef 9

NL–1105 AZ, Amsterdam (The Netherlands)

Tel. +31 20 5665976, Fax +31 20 6968833, E-Mail I.Bank@amc.uva.nl

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Acquired and inherited thrombophilic factors increase the risk for (recurrent) venous thrombotic disease. However, little is known about the pathophysiological mechanisms causing these recurrences, or the persistence of thrombosis despite adequate treatment. Because residual thrombosis has been associated with a worse prognostic outcome, we performed an explorative study in order to investigate the prevalence of residual thrombotic lesions after anticoagulant treatment in patients with deep venous thrombosis. Thrombotic parameters as assessed by ultrasonography after a 12-week course of anticoagulants were used. Both thrombophilia in general and acquired thrombophilia in particular were found to be associated with the extent of residual thrombosis. Of the individual thrombophilic factors, protein C deficiency, prothrombin 20210A mutation, active malignant disease and lupus anticoagulant were associated with an increased risk of residual thrombotic mass. Patients with inherited thrombophilia did not differ from patients without any thrombophilic abnormality with regard to residual thrombotic mass [relative risk (RR) 1.3, 95% confidence interval (CI) 0.9–1.8], while acquired thrombophilic disorders increased the risk for residual thrombotic mass as compared to patients without any defect (RR 1.7, 95% CI 1.2–2.2). Although these results should be confirmed in a larger study, they might help us form hypotheses concerning why patients with thrombophilia are more prone to recurrent venous thromboembolic disease.

© 2004 S. Karger AG, Basel

Article / Publication Details

First-Page Preview
Abstract of Original Paper

Received: February 25, 2004
Accepted: June 22, 2004
Published online: December 02, 2004
Issue release date: July – August

Number of Print Pages: 5
Number of Figures: 0
Number of Tables: 2

ISSN: 1424-8832 (Print)
eISSN: 1424-8840 (Online)

For additional information: http://www.karger.com/PHT

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