Activated protein C resistance, thrombophilia, and inflammatory bowel disease.

1998 
Thromboembolic events frequently complicate theclinical course of patients with inflammatory boweldisease (IBD). Hereditary thrombophilia may contributeto this tendency. Resistance to activated protein C is the most recently described thrombophilicstate and may account for up to 40% of patients withthrombophilia. Thirty-seven patients with IBD werestudied (mean age 44 years, range 18-82 years). Three patients had a history of thrombotic episodes.The 37 controls included 23 men and 17 women (mean age48 years, range 16-89 years). Disease activity wasassessed using the Harvey Bradshaw index for patients with Crohn's disease and the Truelove and Wittsgrading system for patients with ulcerative colitis.Levels of fibrinogen, antithrombin III (ATIII), proteinC, protein S, activated protein C resistance (APCR), and the presence of a lupusanticoagulant (LA) were determined. Median ATIII levelsin patients with IBD were significantly lower thancontrols (98% vs 106%, P = 0.007), while fibrinogen waselevated (4.2 vs 3.3 g/liter, P = 0.026) despitequiescent disease activity. LA was detected in 7/37patients in the IBD group compared to 0/37 controls.(χ2 = 5.68, P = 0.017). No significantdifference was observed in levels of inherited thrombophilic factorsand in particular APCR between IBD patients andcontrols. In conclusion, the presence of inheritedthrombophilic defects, in particular APCR, is uncommonin patients with IBD and does not merit routinescreening.
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