摘要
在过去数十年,大量的研究表明炎性肠病(IBD)患者发展成为心血管疾病的风险正在增加。两者都是慢性炎症疾病,它们的病理生理学机制可能相互影响。IBD病人高水平的细胞因子、C反应蛋白(CRP)和同型半胱氨酸也许会导致内皮功能紊乱,动脉粥样硬化的一种早期迹象。总的来说,IBD病人并没有显示患心血管疾病的典型风险因素,但是其脂质水平的变化却与近期报道的心血管事件很相似。IBD中频繁存在的更高水平的凝血因子,也许会使动脉血栓栓塞事件发生。最终,肠道本身通过其微生物群也许会影响IBD的动脉粥样化形成。微生物产品释放于炎性粘膜,通过肠漏屏障进入循环。诱导的促炎性细胞因子的增加可能会导致内皮损伤、动脉粥样硬化和心血管事件。虽然大量的回顾性研究支持IBD与心血管疾病之间的联系,但是其机制仍旧没被明确。
关键词: 新血管疾病,冠心病,克罗恩病,血脂障碍,木糖醇,脂多糖,血栓栓塞,溃疡性结肠炎
Current Drug Targets
Title:Cardiovascular Complications in Inflammatory Bowel Disease
Volume: 16 Issue: 3
Author(s): Rudolf Schicho, Gunther Marsche and Martin Storr
Affiliation:
关键词: 新血管疾病,冠心病,克罗恩病,血脂障碍,木糖醇,脂多糖,血栓栓塞,溃疡性结肠炎
摘要: Over the past years, a growing number of studies have indicated that patients suffering from inflammatory bowel disease (IBD) have an increased risk of developing cardiovascular disease. Both are chronic inflammatory diseases and share certain pathophysiological mechanisms that may influence each other. High levels of cytokines, C-reactive protein (CRP), and homocysteine in IBD patients may lead to endothelial dysfunction, an early sign of atherosclerosis. IBD patients, in general, do not show the typical risk factors for cardiovascular disease but changes in lipid profiles similar to the ones seen in cardiovascular events have been reported recently. Higher levels of coagulation factors frequently occur in IBD which may predispose to arterial thromboembolic events. Finally, the gut itself may have an impact on atherogenesis during IBD through its microbiota. Microbial products are released from the inflamed mucosa into the circulation through a leaky barrier. The induced rise in proinflammatory cytokines could contribute to endothelial damage, artherosclerosis and cardiovascular events. Although large retrospective studies favor a link between IBD and cardiovascular diseases, the mechanisms behind still remain to be determined.
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Cite this article as:
Rudolf Schicho, Gunther Marsche and Martin Storr , Cardiovascular Complications in Inflammatory Bowel Disease, Current Drug Targets 2015; 16 (3) . https://dx.doi.org/10.2174/1389450116666150202161500
DOI https://dx.doi.org/10.2174/1389450116666150202161500 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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