Biomarkers for post thrombotic syndrome: A case-control study |
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Authors: | A.C. Bouman Y.W. Cheung H.M. Spronk C.G. Schalkwijk H. ten Cate M. ten Wolde A.J. ten Cate-Hoek |
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Affiliation: | 1. Laboratory for Thrombosis and Hemostasis, Maastricht University Medical Centre, Universiteitssingel 50, Maastricht, the Netherlands;2. Department of Internal Medicine, Flevohospital, Hospitaalweg 1, Almere, the Netherlands;3. Department of Internal Medicine, Maastricht University Medical Centre, P.Debyelaan 25, Maastricht, the Netherlands |
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Abstract: | IntroductionThere is limited knowledge on the etiology of post thrombotic syndrome (PTS), although several mechanisms have been proposed.The objectives are to explore the role of different pathogenic mechanisms for PTS, through measurement of an elaborate panel of biomarkers in patients with and without PTS.Materials and MethodsPatients with a history of deep vein thrombosis (DVT) with PTS (cases) and without PTS after minimal 2 years follow-up (controls), were selected from the outpatient clinic of two Dutch hospitals. As a reference to the normal population healthy individuals (HI) without a history of venous thromboembolism were invited to participate. The population consisted of: 26 cases, 27 controls, and 26 HI.A panel of predefined biomarkers was measured in venous blood.ResultsD-dimer showed a decreasing trend from cases to controls to HI; p = 0.010. Thrombin/antithrombin complex levels were significantly higher in cases than in controls; p = 0.032, and HI; p = 0.017. APC-ratio was significantly lower in cases compared to controls; p = 0.032, and HI; p = 0.011. A significant trend of increasing proTAFI from cases, to controls, and HI; p = 0.002 was found. There were no differences in inflammatory markers (CRP, Interleukin-6, Interleukin-8). Thrombomodulin, tissue-plasminogen activator, and von Willebrand factor were higher in patients compared to HI. There was a significant trend of decreasing sVCAM, from cases, to controls, and HI; p = 0.029.ConclusionsPatients with PTS displayed increased coagulation activity, an altered pattern of fibrinolytic marker expression, and increased endothelial activation. We found no evidence of systemic inflammation in patients with PTS at 63 months since the last DVT. |
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Keywords: | A/C, anticoagulant therapy APC, activated protein C CRP, C-reactive protein DVT, deep vein thrombosis ELISA, enzyme-linked immunosorbent assay HI, healthy individuals Il-6/8, interleukin 6/8 IQR, interquartile range MMP-9, matrixmetalloprotease 9 n/a, not applicable PAI-1, tissue-plasminogen activator inhibitor type 1 PAP, plasmin-α-antiplasmin complex proTAFI, pro thrombin activatable fibrinolysis inhibitor PTS, post thrombotic syndrome sICAM-1, soluble intercellular cell adhesion molecule 1 sVCAM-1, soluble vascular cell adhesion molecule 1 TAT, thrombin: antithrombin complex TM, thrombomodulin tPA, tissue plasminogen activator VTE, venous thromboembolism vWF, von Willebrand factor |
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