Factor V Leiden and the etiology of inflammatory bowel disease

Arnold C. Spek; Fiebo J. W. ten Kate; Anje A. te Velde

doi:10.1160/TH07-02-0129

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2007; 98(03): 670-673
DOI: 10.1160/TH07-02-0129

Animal Models

Schattauer GmbH

Factor V Leiden and the etiology of inflammatory bowel disease

Arnold C. Spek

¹Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

,

Fiebo J. W. ten Kate

²Department of Pathology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

,

Anje A. te Velde

¹Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

› Author Affiliations

Abstract

Summary

Inflammatory bowel disease (IBD) refers to two chronic diseases that cause inflammation of the intestines: ulcerative colitis and Crohn’s disease. Patients suffering from IBD have a threefold increased risk of venous thrombosis compared with matched controls. Importantly, thromboembolic disease is a significant cause of morbidity and mortality in patients with IBD. However, despite several supporting observations it is still elusive whether activation of the blood coagulation cascade is involved in the etiology and pathogenesis of IBD. To confirm or refute the hypothesis that activated blood coagulation aggravates the development of IBD, we subjected wildtype and homozygous FV Leiden mice to a model of DSS-induced colitis. Experimental colitis led to a reduction in body weight, shortening of the colon and increased colon weight. In addition, DSS treatment led to ulcerations, edema formation, crypt loss, fibrosis and the influx of inflammatory cells into the colon. However, the FV Leiden genotype had no significant effect on any of the DSS-induced symptoms of colitis. We therefore conclude that the FV Leiden allele has no effect in murine colitis and we thus question the importance of activated blood coagulation in the etiology or pathogenesis of IBD.

Keywords

Animal models - inflammatory mediators - protein C/S pathway

Full Text

References

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