Coagulation and fibrinolysis in inflammatory bowel disease and in giant cell arteritis

A.A. Vrij*, J. Rijken, J.W.J. van Wersch, R.W. Stockbrügger

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Coagulation and fibrinolysis in inflammatory bowel disease and in giant cell arteritis.

Vrij AA, Rijken J, van Wersch JW, Stockbrugger RW.

Department of Gastroenterology, University Hospital, Maastricht, The Netherlands.

BACKGROUND: In inflammatory bowel disease (IBD), gut microvascular thrombosis as well as thromboembolic complications have repeatedly been observed. We examined the long-term course of markers of coagulation and fibrinolysis in relation to clinical disease activity. MATERIALS AND METHODS: In a prospective study, prothrombin fragment 1 and 2 (F1.2), thrombin-antithrombin complex (TAT), antithrombin, D-dimer, plasmin-alpha(2)-antiplasmin complex (PAP) and plasminogen activator inhibitor-1 (PAI-1) were measured in 20 patients with Crohn's disease (CD), 18 with ulcerative colitis (UC), and 19 with giant cell arteritis during active and inactive disease, as well as in 51 controls without inflammation. RESULTS: Levels of F1.2, TAT, D-dimer, PAP and PAI-1 were significantly higher in active versus inactive CD and UC. However, even after 12 months of follow-up, in CD and UC the mean levels of F1.2, D-dimer and PAP were significantly higher than the levels of the controls. CONCLUSIONS: Levels of F1.2, D-dimer and PAP were markedly raised for a long time in clinically inactive IBD, underlining a chronic state of hypercoagulation and enhanced fibrinolysis. Copyright 2003 S. Karger AG, Basel

Original languageEnglish
Pages (from-to)75-83
Number of pages8
JournalPathophysiology of Haemostasis and Thrombosis
Issue number2
Publication statusPublished - 1 Jan 2003

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