胃食管反流病食管上皮损伤的机制  

Mechanisms of esophageal epithelial injury in gastroesophageal reflux disease

作　　者：徐特[1] 张晓琦[1] 邹晓平[1] 

机构地区：[1]南京大学医学院附属鼓楼医院消化内科,江苏省南京市210000

出　　处：《世界华人消化杂志》2014年第21期3030-3035,共6页World Chinese Journal of Digestology

摘　　要：胃食管反流病(gastroesophageal reflux disease,GERD)是消化内科常见的疾病.国内对GERD机制的阐述较集中在引起反流的解剖基础上,如降低的食管下括约肌的张力(lower esophaheal sphincter,LES)、一过性的食管下括约肌的松弛(transient esophaheal sphincter relaxation,tLESR)以及膈疝等,而对于各种反流物:胃酸、胃蛋白酶以及胆汁在存在反流的解剖基础上反流至食管远端引起食管上皮组织学的改变,包括细胞坏死、扩大的细胞间隙增宽(dialeted intercellular space,DIS)、炎症细胞的浸润等改变机制的探讨较少.本文就常见的反流物引起的食管上皮组织损伤的细胞分子层面的机制予以阐述,并且重点介绍、分析近来引起学界广泛关注的免疫损伤机制.Gastroesophageal reflux disease （GERD） is a disease frequently encountered in gastroenterology department. Domestic scholars paid much attention on the anatomical basis of reflux when trying to describe the mechanisms of GERD, such as the decrease of tension of the lower esophageal sphincter （LES） and a transient lower esophageal sphincter （tLESR） and diaphragmatic hernia, and neglected the pathophysiological mechanisms of esophageal epithelial histological changes including cell necrosis, dilated intercellular space （DIS）, and infiltration of inflammatory cells which were induced by the reflux contents including gastric acid, pepsin and bile. In this paper, we will elaborate the mechanisms of esophageal epithelia injury induced by common reflux contents at the cellular and molecular levels, focusing on the introduction and analysis of immune injury mechanism.

关 键 词：胃食管反流病 化学性损伤机制 扩大的细胞间隙 免疫性损伤 

分 类 号：R571[医药卫生—消化系统]