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To provide new concepts regarding the early pathologic changes of gastroesophageal reflux disease (GERD) that are associated with damage to the lower esophageal sphincter (LES).A body of evidence exists that cardiac mucosa is a metaplastic esophageal epithelium rather than a normal gastric epithelium. Recent studies in asymptomatic volunteers suggest a potential mechanism for cardiac metaplasia in the squamous epithelium of the esophagus.The concept that cardiac mucosa is esophageal, not gastric, suggests that the widely accepted endoscopic definition of the gastroesophageal junction (GEJ) is incorrect. I propose that the true GEJ is the proximal extent of gastric oxyntic epithelium. If there is cardiac mucosa lining proximal rugal folds, that cardiac mucosa-lined region is the dilated distal esophagus, not the proximal stomach. The dilated distal esophagus is the pathologic expression of damage to the abdominal segment of the LES. This concept suggests a new test for measuring damage to the abdominal LES and a new understanding of the disease of GERD based on the measured amount of LES damage. This opens the door to new research and change in objectives in the management of reflux disease from control of symptoms to prevention of complications such as Barrett's esophagus and adenocarcinoma.