Thrombin-activatable fibrinolysis inhibitor and its relation with inflammation in rheumatoid arthritis

M J L Peters¹, M T Nurmohamed^1,2, I C van Eijk², C J N Verkleij³, P F Marx³

¹ Department of Rheumatology, VU University Medical Center, Amsterdam, The Netherlands
² Department of Rheumatology, Jan van Breemen Institute, Amsterdam, The Netherlands
³ Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Correspondence to:
P F Marx, Academic Medical Center, Department of Experimental Vascular Medicine, Meibergdreef 9, 1105 AZ (Room G1-145), Amsterdam, The Netherlands; p.f.marx@amc.uva.nl

Accepted 29 September 2008

The first 150 words of the full text of this article appear below.

Rheumatoid arthritis (RA) is associated with an excessive risk of cardiovascular morbidity and mortality, and inflammation appears to be the missing link explaining this markedly elevated risk.¹ Inflammation is a potent inducer of coagulation and fibrinolysis and may contribute to atherosclerotic and thrombotic components of cardiovascular events.² Thrombin-activatable fibrinolysis inhibitor (TAFI), a procarboxypeptidase in plasma, is a regulatory protein of the coagulation/fibrinolysis balance as well as inflammation. TAFIa, the activated form of TAFI, acts by removing C-terminal arginine and lysine residues from substrates such as fibrin degradation products, bradykinin and the anaphylatoxins C3a and C5a. Elevated TAFI levels may reflect an enhanced risk of developing cardiovascular disease, although evidence for this is somewhat contradictory since the use of genotype-sensitive assays complicates interpretation of the data.^3–5 Furthermore, TAFI levels associate with acute phase reactants in patients with cardiovascular disease and are elevated in patients with RA, as compared with non-RA controls.^{6 7} . . . [Full text of this article]

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