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巴雷特食管的病理生理学

Pathophysiology of Barrett's esophagus.

作者信息

Chandrasoma P

机构信息

Department of Surgical Pathology, University of Southern California, Los Angeles 90033, USA.

出版信息

Semin Thorac Cardiovasc Surg. 1997 Jul;9(3):270-8.

PMID:9263345
Abstract

A novel pathophysiology of Barrett's esophagus and a new method of assessing biopsy specimens in patients with gastroesophageal reflux disease (GERD) are presented. This is based on the observation in autopsy studies of patients without GERD that the squamous epithelium of the esophagus transitions directly to fundic mucosa in many people and that the cardiac mucosa is of very short length in others. Available evidence suggests that what is termed gastric cardiac mucosa is in reality an abnormal mucosa resulting from metaplasia of the squamous epithelium of the esophagus as a result of GERD. The severity of GERD correlates with the length of metaplastic cardiac mucosa and further changes occurring in it, permitting development of a system that provides good correlation between biopsy histology and severity of GERD. Intestinal metaplasia ("Barrett's esophagus") always occurs in this metaplastic cardiac mucosa. The recognition of this new pathophysiology of Barrett's esophagus permits identification of the entire sequence whereby GERD leads to adenocarcinoma: GERD-->cardiac metaplasia of squamous epithelium-->reflux carditis-->intestinal metaplasia-->dysplasia-->adenocarcinoma. This article also attempts to develop a terminology that avoids use of the confusing term "Barrett's esophagus," which should be discarded.

摘要

本文介绍了巴雷特食管的一种新的病理生理学以及评估胃食管反流病(GERD)患者活检标本的新方法。这是基于对无GERD患者的尸检研究观察得出的,即食管的鳞状上皮在许多人身上直接转变为胃底黏膜,而在另一些人身上贲门黏膜的长度很短。现有证据表明,所谓的胃贲门黏膜实际上是由于GERD导致食管鳞状上皮化生而产生的异常黏膜。GERD的严重程度与化生的贲门黏膜长度及其进一步发生的变化相关,这使得能够开发出一种系统,该系统能在活检组织学与GERD严重程度之间提供良好的相关性。肠化生(“巴雷特食管”)总是发生在这种化生的贲门黏膜中。认识到巴雷特食管这种新的病理生理学,就能够识别出GERD导致腺癌的整个过程:GERD→食管鳞状上皮贲门化生→反流性食管炎→肠化生→发育异常→腺癌。本文还试图制定一种术语,避免使用容易混淆的“巴雷特食管”一词,该词应予以摒弃。

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