WHAT ARE THE FOLLOW-UP STRATEGIES AFTER ENDOSCOPIC ERADICATION OF BARRETT'S ESOPHAGUS WITH DYSPLASIA AND WHEN TO APPLY THEM?

被引:0
作者
Montero Moreton, A. M. [1 ]
Santos Santamarta, F. [1 ]
Cabezudo Molleda, L. [2 ]
Maestro Antolin, S. [1 ]
Cimavilla Roman, M. [1 ]
Perez Millan, A. G. [1 ]
机构
[1] Complejo Asistencial Univ Palencia, Serv Aparato Digest, Palencia, Spain
[2] Complejo Asistencial Univ Palencia, Serv Med Int, Palencia, Spain
来源
REVISTA CASTELLANA DE GASTROENTEROLOGIA | 2021年 / 36卷 / 03期
关键词
Barrett esophagus; gastroesophageal reflux; adenocarcinoma of esophagus; MANAGEMENT; RECURRENCE; PREDICTORS; GUIDELINE; ABLATION;
D O I
暂无
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Barrett's esophagus (BE) is a change of distal esophageal squamous epithelium to columnar-lined intestinal metaplasia. It is a disease with low prevalence, but whose importance lies in the risk of malignancy to esophagus adenocarcinoma. Gastroesophageal reflux disease is the main risk factor. Diagnosis is endoscopic with histological confirmation by expert pathologists. It is defined according to the Prague classification, assessing both the presence of intestinal metaplasia and visible lesions; For its study, biopsies will be taken according to the Seattle protocol and, independently, analysis of the visible lesions for staging. The follow-up of BE depends mainly on the degree of dysplasia present, and there is a consensus on the review deadlines in national and international societies. The aim of medical treatment is to control gastroesophageal reflux. Endoscopic treatment are ablative and resection techniques, indicated only in cases of confirmed dysplasia in two separate samples. Surgical treatment is indicated in the presence of adenocarcinoma or high-grade dysplasia with submucosal invasion, mainly in cases of poor histological differentiation and lymphovascular dissemination. The surveillance of patients after endoscopic treatment is not clearly established, but there is consensus on the need for periodic surveillance due to the risk of recurrence of intestinal metaplasia, dysplasia and evolution to esophageal adenocarcinoma.
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页码:184 / 188
页数:5
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