Gastroenterology

Gastroenterology

Volume 115, Issue 4, October 1998, Pages 830-834
Gastroenterology

Alimentary Tract
The factor V Leiden mutation increases the risk of venous thrombosis in patients with inflammatory bowel disease,☆☆

https://doi.org/10.1016/S0016-5085(98)70253-7Get rights and content

Abstract

Background & Aims: Thromboembolic disease is a significant cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). The aim of this study was to determine the incidence and possible association of the factor V Leiden mutation with the development of thrombosis in patients with IBD. Methods: This retrospective study included 11 patients with IBD and arterial or venous thrombosis and 51 patients with IBD and no history of thrombosis who were matched for age, sex, ethnic/racial origin, and type of IBD (controls). The presence of the factor V Leiden mutation was determined by coagulation assay and confirmed by a polymerase chain reaction method. Results: Four of 11 IBD patients (36%) with thrombosis and 2 of 51 IBD controls (4%) were heterozygotes for the factor V Leiden mutation (relative risk, 14.00; 95% confidence interval, 1.55-169.25; P = 0.009, Fisher exact test). All thrombotic events in the patients with activated protein C resistance were venous with a calculated prevalence of 50% (4 of 8 patients) and a relative risk of venous thrombosis in IBD patients with factor V Leiden of 23 (95% confidence interval, 2-294; P = 0.005). Conclusions: In patients with IBD, inheritance of the factor V Leiden mutation results in a significant increased risk of venous thrombosis.

GASTROENTEROLOGY 1998;115:830-834

Section snippets

Materials and methods

The study population included 11 patients with a history of IBD and thromboembolic complications and 51 IBD controls. A review of the records from Los Angeles County–University of Southern California (LAC-USC) Medical Center Anticoagulation Clinic, the IBD clinic, and hematology consultation records identified 14 patients with IBD and a history of either arterial or venous thrombosis. Only 11 of these patients were available to perform studies for APCR and factor V Leiden. A control population

Results

The characteristics of the study populations are shown in Table 1. There were no significant differences in age or sex between the IBD patients with thrombosis and patients without thrombosis. The average age of the patients with IBD at the time of their thrombotic event was 39 years (range, 21-64 years), and the patients were studied an average of 2.5 months (range, 4 days to 36 months) after their thromboembolic event. Ulcerative colitis was the most frequent form of IBD in patients with

Discussion

Thromboembolic complications are a rare but a significant complication of IBD. The reported incidence of thrombosis in three large retrospective studies was approximately 1.3%-6.4%.1, 4, 5 However, the contribution of thromboembolic complications to patient morbidity and mortality is significant. In the study by Talbot et al.,5 23 of 92 patients (25%) with documented thromboembolic complications died during their acute episodes. Therefore, a better understanding of the mechanisms contributing

References (43)

  • WE Ricketts et al.

    Complications of chronic non-specific ulcerative colitis

    Gastroenterology

    (1946)
  • C Dennis et al.

    Surgical measures as supplements to the management of idiopathic ulcerative colitis: cancer, cirrhosis and arthritis as frequent complications

    Surgery

    (1952)
  • FC Edwards et al.

    The course and prognosis of ulcerative colitis. Part III. Complications

    Gut

    (1964)
  • S Warren et al.

    Pathogenesis of ulcerative colitis

    Am J Pathol

    (1949)
  • V Graef et al.
  • M Hudson et al.

    Evidence for activation of coagulation in Crohn's disease

    Blood Coag Fibrinol

    (1992)
  • TRJ Stevens et al.

    Circulating von Willebrand factor in inflammatory bowel disease

    Gut

    (1992)
  • JC Souto et al.

    Prothrombotic state and signs of endothelial lesion in plasma of patients with inflammatory bowel disease

    Dig Dis Sci

    (1995)
  • B Dahlback et al.

    Familial thrombophilia due to a previously recognized mechanism characterized by poor anticoagulant response to activated protein C: prediction of a cofactor to activated protein C

    Proc Natl Acad Sci USA

    (1993)
  • NJ Beauchamp et al.

    High prevalence of a mutation in the factor V gene within the U.K. population: relationship to activated protein C resistance and familial thrombosis

    Br J Haematol

    (1994)
  • PJ Svensson et al.

    Resistance to activated protein C as a basis for venous thrombosis

    N Engl J Med

    (1994)
  • Cited by (99)

    • Ulcerative Colitis

      2010, Sleisenger and Fordtran’s Gastrointestinal and Liver Disease- 2 Volume Set: Pathophysiology, Diagnosis, Management, Expert Consult Premium Edition - Enhanced Online Features and Print
    • Inflammatory Bowel Disease and Strokes

      2018, Uncommon Causes of Stroke: Third Edition
    View all citing articles on Scopus

    Address requests for reprints to: Howard A. Liebman, M.D., Department of Medicine and Pathology, University of Southern California School of Medicine, Kenneth Norris Jr. Cancer Hospital, Topping Tower, Third Floor, 1441 Eastlake Avenue, Los Angeles, California 90033. e-mail: [email protected]; fax: (213) 764-0060.

    ☆☆

    Supported in part by grant 987 F1-2 from the American Heart Association Greater Los Angeles Chapter (to H.A.L.).

    View full text