New evidence defining the pathology and pathogenesis of lower esophageal sphincter damage

Parakrama Chandrasoma

doi:10.1007/s10353-019-00616-0

Abstract

SummaryBackgroundPresent diagnosis and management of gastroesophageal reflux disease (GERD) has resulted in a dramatic increase in the incidence of esophageal adenocarcinoma. This is due to failure to identify pathologic changes of early GERD; at present, pathology is limited to management of Barrett esophagus (BE).MethodsConvincing evidence have confirmed that cardiac mucosa distal to the squamocolumnar junction in the endoscopically normal person is a metaplastic GERD-induced esophageal epithelium, and not a normal proximal gastric epithelium.ResultsWhen cardiac mucosa is recognized as a metaplastic esophageal epithelium, it becomes self-evident that the present endoscopic definition of the gastro-esophageal junction is incorrect, and there exists a dilated distal esophagus (DDE) in what is incorrectly termed the “gastric cardia” presently mistaken for proximal stomach. It also becomes clear that the length of the DDE correlates with the presence and severity of GERD and represents the pathology of the entire spectrum of GERD. Further, it allows recognition that the DDE, measured as the gap between esophageal squamous epithelium and gastric oxyntic mucosa that is composed of cardiac mucosa, represents the pathologic anatomy of damage to the abdominal segment of the lower esophageal sphincter (LES).ConclusionThe new understanding of the significance of cardiac mucosa provides a new and highly accurate histologic method of assessment of LES damage, the primary cause of GERD. This opens a new door to complete histologic assessment of GERD from its etiologic standpoint and to new research that permit early diagnosis of GERD at its outset. Ultimately, such early diagnosis has the potential to reverse the increasing trend of esophageal adenocarcinoma.

Highlights

Gastroesophageal reflux disease (GERD) is a common human disease
In a study of autopsies in 18 persons without clinical GERD during life [12], we showed that pure cardiac mucosa was absent in 10/18 (56%)
This study showed that the small amounts of cardiac mucosa found in these asymptomatic volunteers was similar to non-intestinalized columnar epithelium in Barrett esophagus (BE) [22]

Summary

Introduction

Gastroesophageal reflux disease (GERD) is a common human disease. In the Western world, it has a prevalence of 30% [1]. The cause of GERD is conceptually simple: it results when the mechanism that normally prevents reflux of gastric contents into the esophagus fails. In a patient with a competent LES, reflux does not occur. Despite this obvious etiology, present medical management is largely aimed at suppressing gastric acid secretion with a naïve and incorrect belief that the disease will be cured by making the refluxed gastric juice less acidic. No amount of acid in the stomach will cause GERD if the LES is competent. No amount of acid suppression will cure reflux if the LES is defective. Patients with GERD who are treated with acid suppressive therapy continue to reflux gastric contents of higher pH, i.e., weak acid reflux [2]

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Conclusion