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Platelets and Anticoagulant Capacity in Patients with Inflammatory Bowel DiseaseLarsen T.B.a · Nielsen J.N.b · Fredholm L.b · Lund E.D.b · Brandslund I.b · Munkholm P.c · Hey H.d
aDepartment of Clinical Biochemistry, Section for Thrombosis and Hemostasis, Aalborg Hospital, Aalborg, bDepartment of Clinical Biochemistry, Vejle County Central Hospital, Vejle, cDepartment of Medical Gastroenterology, University Hospital of Copenhagen, Copenhagen, and dDepartment of Medical Gastroenterology, Vejle County Central Hospital, Vejle, Denmark Corresponding Author
Torben Bjerregaard Larsen, MD, PhD
Department of Clinical Biochemistry, Section for Thrombosis and Hemostasis
Aalborg Hospital, Hobrovej 18–22, PO Box 365
DK–9100 Aalborg (Denmark)
Tel. +45 9932 3180, Fax +45 9813 1196, E-Mail firstname.lastname@example.org
Patients with inflammatory bowel disease (IBD) are susceptible to thromboembolic complications. Several mechanisms can be responsible, including abnormal regulation of coagulation activity, disturbances of fibrinolysis, inflammatory reactions and thrombocytosis. The aim of this study was to assess hemostatic alterations in these parameters during exacerbation of disease. We studied disease activity in 99 IBD patients receiving anti-inflammatory therapy, in relation to: procoagulant markers, i.e. prothrombin fragment F1 + 2 (F1 + 2), D-dimer and platelet count, anticoagulant markers, i.e. protein C, protein S and antithrombin, and a mediator of inflammation (IL-6). Coagulation activity and platelet count were increased during active disease in IBD patients compared with those in a state of remission. The IL-6 concentrations were positively correlated with disease activity and thrombocytosis in patients with ulcerative colitis, but no association with the anticoagulant capacity could be demonstrated except for a decrease in protein C during high disease activity.
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