克罗恩病肠壁纤维化机制研究进展  

Research progress in mechanisms of intestinal fibrosis in Crohn’s disease

作　　者：戴萌[1] 李弼民[1] 

机构地区：[1]南昌大学第一附属医院消化内科,江西省南昌市330006

出　　处：《世界华人消化杂志》2009年第11期1117-1121,共5页World Chinese Journal of Digestology

摘　　要：正常组织修复与慢性炎症、脏器纤维化之间的关系尚不明确,急性炎症可导致正常间质细胞转化为纤维化型,但如果急性炎症转化为慢性炎症且异常持续下去,则会导致纤维化.克罗恩病(Crohn'sdisease,CD)患者的肠壁慢性炎症可导致肠道产生大量细胞外基质沉积,从而引起瘢痕收缩式狭窄.目前CD中肠道纤维化机制尚不明确且临床尚无有效的治疗方案,有关CD肠壁纤维化的研究日益引起重视.本文就CD肠壁纤维化的发病机制的研究进展作一概述.The relationship between fibrosis and normal repair are not understood. Acute injury may cause normal mesenchymal cells to convert to fibrogenic phenotype that may lead to fibrosis when inappropriately sustained. Crohn＇s disease （CD）-associated fibrosis results from chronic transmural inflammation. Intestinal inflammation in CD is transmural, often associated with extracellular matrix changes, luminal narrowing and stricture formation. But the pathogenesis of stricture formation remains unclear. Current therapies do not alter its progression to intestinal fibrosis and obstruction. The aim of this review is to discuss the current understanding of fibrogenesis in CD.

关 键 词：克罗恩病 肠壁纤维化 炎症性肠病 溃疡性结肠炎 

分 类 号：R574[医药卫生—消化系统]