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Abstract: Background: Circulating procoagulant microparticles (MPs) are thought to be involved in the pathogenesis of venous thromboembolism in patients with inflammatory bowel disease (IBD). However, the exposure of tissue factor, the primary initiator of coagulation activation, on microparticles (TF+MPs) and its association with hemostasis activation has not yet been studied in IBD patients. Methods: In this case–control study 49 IBD patients (28 Crohn''s disease, 21 ulcerative colitis) and 49 sex- and age-matched, healthy controls were included. Clinical disease activity (Crohn''s Disease Activity Index and Clinical Activity Index, respectively) was assessed and IBD-related data were determined by chart review. Numbers, cellular origin and procoagulant activity of TF+MPs in plasma were determined using flow cytometry and a chromogenic activity assay. D-dimer and high-sensitive C-reactive protein (CRP) served as markers for coagulation activation and inflammation, respectively. The primary endpoint was the number of TF+MPs in IBD patients compared to controls. Results: Median number (interquartile range) of TF+MPs was higher in IBD patients than in controls (14.0 (11.9–22.8)×103/mL vs. 11.9 (11.9–19.1)×103/mL plasma, P=0.029). This finding was due to generally higher plasma levels of MPs from platelets and leukocytes in IBD patients. However, the number of TF+MPs was neither correlated with their procoagulant activity and D-dimer nor with disease activity and CRP. Conclusions: Increased numbers of circulating TF+MPs represent a new facet of hemostatic abnormalities in IBD. However, the lack of association with activation of the coagulation system and disease activity questions their pathogenetic role for venous thromboembolism in this patient group. [Copyright &y& Elsevier]

Eur J Clin Invest 2010; 40 (6): 477–482 Background Microparticles (MPs) have procoagulant properties as shown in vitro and in animal models. Their role in haemostatic system activation at the site of a vascular injury in vivo in humans has not been studied. Material and methods In a prospective randomized crossover study, 13 healthy volunteers were given 100 mg acetylsalicylic acid or placebo daily for 7 days. Number and cellular origin, expression of tissue factor (TF) and phosphatidylserine on MPs, and platelet and coagulation activation markers [β-thromboglobulin (β-TG), prothrombin fragment f1·2 (f1·2)] were measured in venous blood and in blood from a vascular injury (shed blood) by flow cytometry and immunoassays, respectively. Results The number of MPs was significantly higher in shed blood than in venous blood. The majority of MPs were platelet derived. The expression of TF on MPs was low, but higher in shed blood than in venous blood. TF positive MPs were significantly higher in shed blood, which was due to an increase of MPs from platelets (PMPs). In shed blood, the number of TF expressing platelet-derived MPs correlated with β-TG, but not with f1·2. Low dose acetylsalicylic acid did not affect shedding of PMPs, neither in venous blood nor in shed blood. Conclusions The release of PMPs locally at the site of platelet plug formation in humans indicates a possible role of MPs for haemostatic system activation in vivo. Low dose acetylsalicylic acid might not be strong enough to suppress shedding of PMPs in the microcirculation. [ABSTRACT FROM AUTHOR]