Mourad Fadi H, Barada Kassem A, Saade Nayef E
Department of Anatomy, Cell Biology and Physiology, American University of Beirut, Beirut-Lebanon.
Department of Internal Medicine, American University of Beirut, Beirut-Lebanon.
J Crohns Colitis. 2017 Mar 1;11(3):369-377. doi: 10.1093/ecco-jcc/jjw162.
Small intestinal dysfunction has been described in patients with ulcerative colitis and in experimental animal models of colitis. This is demonstrated by a decrease in fluid, electrolyte, amino acid, fat and carbohydrate absorption as well as by deranged intestinal motility. Histopathological changes in the small intestines in colitis have not been consistently demonstrated, but there is evidence of structural and biochemical alterations as shown by increased intestinal permeability and a decrease in the expression of multiple brush border membrane enzymes such as disaccharidases and aminopetidases, in both humans and experimental animals. The pathophysiology of this dysfunction has not been elucidated, but it is thought to include alterations in neural circuitry such as increased neuronal excitability, neuronal damage and changes of neuropeptidergic innervation and receptors as well as an increase in local production of pro-inflammatory cytokines and alterations in the production of some neurohumoral mediators. In the following, we provide an update on the advancement of clinical and scientific contributions to elucidate the underlying mechanisms of the alteration of the functions of apparently intact small intestinal segments, induced by ulcerative colitis.
溃疡性结肠炎患者以及结肠炎实验动物模型中均出现过小肠功能障碍。这表现为液体、电解质、氨基酸、脂肪和碳水化合物吸收减少以及肠道运动紊乱。结肠炎患者小肠的组织病理学变化尚未得到一致证实，但在人类和实验动物中均有证据表明存在结构和生化改变，如肠道通透性增加以及多种刷状缘膜酶（如双糖酶和氨基肽酶）的表达减少。这种功能障碍的病理生理学尚未阐明，但据认为其包括神经回路的改变，如神经元兴奋性增加、神经元损伤以及神经肽能神经支配和受体的变化，以及促炎细胞因子局部产生增加和一些神经体液介质产生的改变。在下文中，我们提供了关于临床和科学贡献进展的最新情况，以阐明溃疡性结肠炎引起的明显完整小肠段功能改变的潜在机制。
