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Venous thrombosis in inflammatory bowel disease

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LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00042737-200507000-00001

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factor V Leiden; hyperhomocysteinemia; platelet activation; prothrombin gene mutation; tissue factor-bearing microvesicles

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Patients with inflammatory bowel disease (IBD) have a threefold increased risk of venous thrombosis, a major cause of morbidity and mortality. Although the exact mechanism explaining the initiation of thrombosis remains unclear, it is likely to be a multifactorial process. Reported abnormalities include activation of markers of the coagulation cascade, disturbed fibrinolysis and the activation of platelets. The contribution of thrombophilic disorders such as factor V Leiden, prothrombin gene mutations and hyperhomocysteinaemia are discussed, but their role in thrombosis associated with IBD has remained unclear. Recent research has examined elevated CD40, P-selectin levels and tissue factor-bearing microvesicles in venous thrombosis, and the relevance of these observations to IBD is reviewed.

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