Patients with Antineutrophil Cytoplasmic Antibodies Associated Vasculitis in Remission Are Hypercoagulable

Marc Hilhorst, Kristien Winckers, Benjamin Wilde, Rene van Oerle, Hugo ten Cate, Jan Willem Cohen Tervaert*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Objectives. The risk of venous thromboembolism (VTE) is increased in patients with antineutrophil cytoplasmic antibodies (ANCA) associated vasculitides (AAV) as compared to healthy subjects. The mechanisms underlying this increased occurrence of VTE are not completely understood. We hypothesize that AAV patients in remission are more procoagulant than healthy controls. Methods. Patients with AAV in remission and no VTE for the last 6 months were included. Patients with severe renal impairment (serum creatinine > 250 mu mol/l) were excluded. Age and sex matched healthy controls were included. The endogenous thrombin potential (ETP) was determined together with hemostatic variables: fibrinogen, D-dimers, factor VIII (FVIII), tissue factor pathway inhibitor (TFPI), protein C, and free protein S. Results. Thirty-one patients were included. In 27 patients not taking anticoagulants, ETP was measured and found to be elevated: 137.1% as compared to a median of 90.0% for healthy controls (p <0.01). Fibrinogen and D-dimer levels were not elevated in patients (median 35 g/l and 279 mu g/l, respectively). FVIII and TFPI levels were also significantly increased in patients as compared to healthy controls (159% vs 137%; 122.5% vs 101%, respectively), whereas protein C and free protein S levels were not elevated (126.5% vs 118.6% and 124.6% vs 118.3%, respectively). Conclusion. Patients with AAV in remission are more procoagulant than healthy controls, as indicated by an increased ETP. The increased FVIII level measured in these patients suggests persistence of endothelial activation and/or dysfunction. This endothelial dysfunction may cause a continuous low-grade procoagulant state.
Original languageEnglish
Pages (from-to)2042-2046
JournalJournal of Rheumatology
Issue number12
Publication statusPublished - Dec 2013



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