Acid suppression and reepithelialization after ablation of Barrett's esophagus

The role of acid reflux in the development of esophageal columnar epithelium was first described in the early 1970s in the canine esophageal reflux model. In the presence of acid reflux, columnar epithelium developed at the site of induced esophageal mucosal injury. When reflux was suppressed, most epithelium reverted back to squamous mucosa. Similar findings in human patients with Barrett's esophagus (BE) who were treated with laser ablation were first described in 1993. While acid suppression with antireflux surgery or proton pump inhibitors (PPIs) has proven insufficient to completely reverse BE, ablation of the lesion followed by acid suppression may be a promising option. Although at least one report disputes the importance of complete acid suppression following mucosal ablation of BE, most investigators use full-dose PPI therapy following ablation, in the belief that full acid suppression provides an environment that allows the esophageal progenitor cell to develop squamous mucosa. This article provides a review of the literature to date regarding ablative therapies and acid suppression for patients with BE.