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Thrombin-activatable fibrinolysis inhibitor and its relation with inflammation in rheumatoid arthritis
  1. M J L Peters1,
  2. M T Nurmohamed1,2,
  3. I C van Eijk2,
  4. C J N Verkleij3,
  5. P F Marx3
  1. 1
    Department of Rheumatology, VU University Medical Center, Amsterdam, The Netherlands
  2. 2
    Department of Rheumatology, Jan van Breemen Institute, Amsterdam, The Netherlands
  3. 3
    Department of Experimental Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
  1. P F Marx, Academic Medical Center, Department of Experimental Vascular Medicine, Meibergdreef 9, 1105 AZ (Room G1-145), Amsterdam, The Netherlands; p.f.marx{at}amc.uva.nl

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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 …

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