Barrett Esophagus In general, esophagitis in the presence of Barrett esophagus can be easily healed with PPI therapy, but meaningful regression of Barrett epithelium, except for small squamous islands, is rarely reported even with high-dose PPI therapy. Recent ex vivo studies have suggested that intermittent “pulses” of acid result in enhanced Barrett epithelial cell proliferation, possibly increasing the risk of dysplasia and cancer. Some have suggested the need to eliminate all acid reflux in patients with Barrett esophagus, but this would require high and frequent doses of expensive medications and serial pH monitoring to document efficacy of therapy. Pending further clinical studies, patients with Barrett esophagus should be treated like others with chronic GERD. Esophageal resection of Barrett esophagus can prevent the progression to cancer, but this requires a total esophagectomy with high mortality, except in selected surgical centers. Therefore, ablation of Barrett epithelium in the setting of strict PPI anacidity has been proposed. Photodynamic therapy, laser, multipolar electrocoagulation, argon plasma coagulation, and endoscopic mucosal resection have been used for this purpose. In these studies, Barrett mucosa can be reversed completely in 70% to 80% of patients, but intestinal metaplasia underlying the new squamous mucosa is reported in almost all series, with the occasional residual foci of metaplasia developing adenocarcinoma. Adverse effects of ablation therapy have ranged from mild chest pain, sore throat, or odynophagia to esophageal perforation and death. The incidence of adenocarcinoma in patients with Barrett esophagus without dysplasia is probably so low that endoscopic ablation cannot be advocated outside of study protocols. Endoscopic therapy for patients with high-grade dysplasia or early cancer holds more promise, especially in the older patients with comorbid illnesses. Because there is currently no way of eliminating the malignant risk of Barrett esophagus, regular endoscopic surveillance is recommended. Biopsies should be taken from each quadrant every 2 cm axially within the metaplastic tissue. The rationale is that dysplasia within Barrett epithelium is often multifocal, and obtaining fewer tissue samples increases the risk of missing dysplastic areas. Brush cytology can compliment endoscopic biopsies. Biomarkers, such as p53, and flow cytometry may augment the yield of histological examination of biopsy specimens. Although prospective studies are not available, case series confirm that esophageal adenocarcinomas detected by endoscopic surveillance are at an earlier stage with a more favorable survival than cancers detected at the time of diagnosis of Barrett, typically when patients present with dysphagia. The appropriate surveillance interval for patients with Barrett esophagus has not been studied prospectively. However, current programs, such as proposed by the
Labels: Barrett’s Esophagus