The Columnar Lined Esophagus. Pathophysiological and Clinical Aspects

Abstract: There is a persisting controversy concerning the definition, etiology and pathogenesis of Barrett's esophagus. The dramatic and parallel increase in the incidence of esophageal and junctional adenocarcinoma over the past decades justifies an evaluation of the pathophysiology of premalignant metaplastic changes of the esophagus and the gastroesophageal junction. Patients were evaluated with upper GI endoscopy, esophageal manometry, and 24-hour esophageal pH and bilirubin monitoring. Biopsies were obtained from areas of esophageal columnar mucosa (ECM) and from just below the squamocolumnar junction (SCJ). Clinical data and results of esophageal function tests were related to the endoscopic and histologic findings. The presence of cardiac mucosa, with and without inflammation and intestinal metaplasia (IM) in biopsies from just below a normal appearing SCJ were associated with the hallmarks of gastroesophageal reflux disease (GERD). Patients with short segment Barrett's esophagus (SSBE) had similar but less profound abnormalities in the antireflux mechanism and in esophageal acid and bilirubin exposure compared to patients with traditional Barrett's esophagus (BE). Increasing length of cardiac mucosa with IM was associated with deterioration of the lower esophageal sphincter and increasing degree of esophageal acid exposure. Patients with IM within ECM had similar esophageal acid exposure but significantly longer duration of reflux symptoms and a higher prevalence of abnormal bilirubin exposure compared to patients without IM. During endoscopic surveillance, the prevalence of IM increased with increasing length of the ECM and with increasing number of surveillance endoscopies. Patients with surgically treated GERD were 10.3 times less likely to develop IM compared to patients receiving medical therapy. Following esophagectomy and gastric tube reconstruction, ECM was found significantly more often in the cervical esophagus in patients with a preoperative diagnosis of BE. Cardiac mucosa, with and without inflammation and IM may be manifestations of gastroesophageal reflux. SSBE is a complication to GERD and a manifestation of the same underlying disease process as traditional BE. The extent of cardiac mucosa with IM is determined by the severity of GERD. ECM, regardless of histologic type is a manifestation of GERD. The presence of duodenoesophageal reflux and the duration of reflux may be important factors in the pathogenesis of IM. Patients with surgically treated GERD developed IM significantly less frequent than patients receiving standard medical therapy. ECM most likely develops in response to squamous epithelial injury in patients with the required underlaying genetic traits.