Pathophysiology of IBD associated diarrhea.
Pathophysiology of IBD associated diarrhea.
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DOI：
10.1080/21688370.2018.1463897
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发表时间：
2018
期刊：
影响因子：
3.1
通讯作者：
Dudeja PK
中科院分区：
文献类型：
--
作者：
Anbazhagan AN;Priyamvada S;Alrefai WA;Dudeja PK
炎症性肠病广泛分为克罗恩病（CD）和溃疡性结肠炎（UC），是胃肠道的慢性炎症性疾病，在全球范围内的患病率不断增加。该疾病的病因是复杂的，涉及遗传、环境、免疫和肠道微生物因素的组合。反复出血性腹泻是IBD中最普遍和最令人衰弱的症状。IBD相关性腹泻的发病机制是多因素的，基本上是由持续性炎症引起的粘膜损伤的结果，导致肠离子转运失调、上皮屏障功能受损和病原体对肠粘膜的可及性增加。上皮离子转运蛋白和通道的表达和/或功能改变是肠腔中电解质潴留和水积聚导致IBD腹泻的主要原因。异常的屏障功能通过漏流机制进一步促进腹泻。肠道病原体的粘液渗透促进生态失调并加剧潜在的免疫系统，进一步使IBD相关的组织损伤和腹泻永久化。在这里，我们回顾了离子转运受损和上皮屏障功能丧失导致IBD相关腹泻的机制。
Inflammatory bowel diseases broadly categorized into Crohn's disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the gastrointestinal tract with increasing prevalence worldwide. The etiology of the disease is complex and involves a combination of genetic, environmental, immunological and gut microbial factors. Recurring and bloody diarrhea is the most prevalent and debilitating symptom in IBD. The pathogenesis of IBD-associated diarrhea is multifactorial and is essentially an outcome of mucosal damage caused by persistent inflammation resulting in dysregulated intestinal ion transport, impaired epithelial barrier function and increased accessibility of the pathogens to the intestinal mucosa. Altered expression and/or function of epithelial ion transporters and channels is the principle cause of electrolyte retention and water accumulation in the intestinal lumen leading to diarrhea in IBD. Aberrant barrier function further contributes to diarrhea via leak-flux mechanism. Mucosal penetration of enteric pathogens promotes dysbiosis and exacerbates the underlying immune system further perpetuating IBD associated-tissue damage and diarrhea. Here, we review the mechanisms of impaired ion transport and loss of epithelial barrier function contributing to diarrhea associated with IBD.