Papa Alfredo, Scaldaferri Franco, Danese Silvio, Guglielmo Simona, Roberto Italia, Bonizzi Michele, Mocci Giammarco, Felice Carla, Ricci Caterina, Andrisani Gianluca, Fedeli Giuseppe, Gasbarrini Giovanni, Gasbarrini Antonio
Department of Internal Medicine, Division of Gastroenterology, Catholic University of Rome, Rome, Italy.
Dig Dis. 2008;26(2):149-55. doi: 10.1159/000116773. Epub 2008 Apr 21.
Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel disease (IBD), are chronic inflammatory conditions, characterized by a microvascular and also macrovascular involvement. Chronically inflamed intestinal microvessels of IBD patients have demonstrated significant alterations in their physiology and function compared with vessels from healthy and uninvolved IBD intestine. Recently, some studies have revealed that the poor mucosal healing, refractory inflammatory ulcerations and damage in the IBD intestine could depend on microvascular dysfunction, resulting in diminished vasodilatory capacity and tissue hypoperfusion in the IBD gut. Furthermore, several data show that the activation of intestinal endothelium plays a critical role in the pathogenesis and/or in perpetuating and amplifying the inflammatory process in IBD and, consequently, it is now emerging as a potential use of anticoagulant or coagulation-related drugs in treating IBD. IBD is also associated with an increased risk of macrovascular venous and arterial thrombosis. Thrombotic events occur prevalently as deep vein thrombosis and pulmonary embolism. They happen at an earlier age than in non-IBD patients. Prothrombotic risk factors in IBD patients could be distinguished as acquired, such as active inflammation, immobility, surgery, steroid therapy, and use of central venous catheters, and inherited. Furthermore, it has been found that IBD, per se, is an independent risk factor for thrombosis. The prevention of thromboembolic events in IBD patients includes the elimination of removable risk factors and, if thrombosis occurs, a pharmacological therapy similar to that used for thromboembolic events occurring in the general population.
克罗恩病（CD）和溃疡性结肠炎（UC）是炎症性肠病（IBD）的两种主要形式，是慢性炎症性疾病，其特征是微血管和大血管均受累。与来自健康且未受累的IBD肠段的血管相比，IBD患者慢性炎症的肠道微血管在生理和功能上已显示出显著改变。最近，一些研究表明，IBD肠道中黏膜愈合不良、难治性炎性溃疡和损伤可能取决于微血管功能障碍，导致IBD肠道血管舒张能力减弱和组织灌注不足。此外，多项数据表明，肠道内皮细胞的激活在IBD发病机制和/或炎症过程的持续及放大中起关键作用，因此，抗凝或凝血相关药物在治疗IBD方面正逐渐成为一种潜在的应用。IBD还与大血管静脉和动脉血栓形成风险增加有关。血栓事件主要表现为深静脉血栓形成和肺栓塞。它们比非IBD患者发病年龄更早。IBD患者的血栓形成危险因素可分为获得性因素，如活动性炎症、活动减少、手术、类固醇治疗和中心静脉导管的使用，以及遗传性因素。此外，已发现IBD本身就是血栓形成的独立危险因素。IBD患者血栓栓塞事件的预防包括消除可去除的危险因素，若发生血栓形成，则采用与一般人群中发生的血栓栓塞事件相同的药物治疗。
