Spek C Arnold, ten Kate Fiebo J W, te Velde Anje A
Center for Experimental and Molecular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
Thromb Haemost. 2007 Sep;98(3):670-3. doi: 10.1160/th07-02-0129.
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 three-fold 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.
炎症性肠病（IBD）指的是两种导致肠道炎症的慢性疾病：溃疡性结肠炎和克罗恩病。与配对的对照组相比，患有IBD的患者发生静脉血栓形成的风险增加了两倍。重要的是，血栓栓塞性疾病是IBD患者发病和死亡的重要原因。然而，尽管有多项支持性观察结果，但凝血级联反应的激活是否参与IBD的病因和发病机制仍不明确。为了证实或反驳激活的凝血会加重IBD发展这一假说，我们将野生型和纯合子FⅤ莱顿小鼠用于葡聚糖硫酸钠（DSS）诱导的结肠炎模型。实验性结肠炎导致体重减轻、结肠缩短和结肠重量增加。此外，DSS治疗导致溃疡、水肿形成、隐窝丢失、纤维化以及炎症细胞流入结肠。然而，FⅤ莱顿基因型对任何DSS诱导的结肠炎症状均无显著影响。因此，我们得出结论，FⅤ莱顿等位基因在小鼠结肠炎中没有作用，因此我们质疑激活的凝血在IBD病因或发病机制中的重要性。
