Activated protein C resistance, thrombophilia, and inflammatory bowel disease

Thromboembolic events frequently complicate the clinical course of patients with inflammatory bowel disease (IBD). Hereditary thrombophilia may contribute to this tendency. Resistance to activated protein C is the most recently described thrombophilic state and may account for up to 40% of patients...

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Bibliographic Details
Published in:Digestive diseases and sciences 1998-06, Vol.43 (6), p.1356-1361
Main Authors: HENEGHAN, M. A, CLEARY, B, MURRAY, M, O'GORMAN, T. A, MCCARTHY, C. F
Format: Article
Language:English
Subjects:
Adolescent
Adult
Aged
Aged, 80 and over
Antithrombin III - analysis
Biological and medical sciences
Biomarkers
Female
Gastroenterology. Liver. Pancreas. Abdomen
Hemostasis
Humans
Inflammatory Bowel Diseases - complications
Inflammatory Bowel Diseases - physiopathology
Male
Medical sciences
Middle Aged
Other diseases. Semiology
Partial Thromboplastin Time
Protein C - metabolism
Protein S - metabolism
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Thrombophilia - etiology
Thrombophilia - physiopathology
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Summary:Thromboembolic events frequently complicate the clinical course of patients with inflammatory bowel disease (IBD). Hereditary thrombophilia may contribute to this tendency. Resistance to activated protein C is the most recently described thrombophilic state and may account for up to 40% of patients with thrombophilia. Thirty-seven patients with IBD were studied (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 age 48 years, range 16-89 years). Disease activity was assessed using the Harvey Bradshaw index for patients with Crohn's disease and the Truelove and Witts grading system for patients with ulcerative colitis. Levels of fibrinogen, antithrombin III (ATIII), protein C, protein S, activated protein C resistance (APCR), and the presence of a lupus anticoagulant (LA) were determined. Median ATIII levels in patients with IBD were significantly lower than controls (98% vs 106%, P = 0.007), while fibrinogen was elevated (4.2 vs 3.3 g/liter, P = 0.026) despite quiescent disease activity. LA was detected in 7/37 patients in the IBD group compared to 0/37 controls. (chi2 = 5.68, P = 0.017). No significant difference was observed in levels of inherited thrombophilic factors and in particular APCR between IBD patients and controls. In conclusion, the presence of inherited thrombophilic defects, in particular APCR, is uncommon in patients with IBD and does not merit routine screening.
ISSN:0163-2116
1573-2568
DOI:10.1023/A:1018840715357