Surgical therapy for Barrett's esophagus: prevention, protection and excision.

Barrett’s esophagus is a complication of gastroesophageal reflux disease and is a manifestation of chronic tissue injury. It is characterized by the presence of intestinal metaplasia in an esophagus lined with cardiac-type mucosa; alternatively described as a columnar-lined esophagus with intestinal metaplasia or Barrett’s mucosal. When present, the abnormal mucosa confers a more than 30 to125-fold risk of progression to esophageal adenocarcinoma, which emerges at a rate of about 1–2 cancers per 100 patient-years of follow-up. Current dogma states that Barrett’s esophagus develops quickly to its full extent, with little subsequent increase in length. This is based on data from patients with only long segments of Barrett’s mucosa within the tubular esophagus, i.e. >3 cm. It is now accepted that intestinal metaplasia occurs in segments of cardiac-type mucosa that are less than 3 cm in length, and that intestinal metaplasia can even occur in extremely small segments of cardiactype mucosa located just below the squamous epithelium of an endoscopically normal appearing gastroesophageal junction. It is known that cardiac-type mucosal at the gastroesophageal junction is almost always inflamed, as evident by an inflammatory infiltrate on microscopy, and is exposed to increased acid exposure on 24 h esophageal pH monitoring. Consequently, this finding is referred to as carditis and is one of the early signs of gastroesophageal reflux disease. The length of the inflamed cardiac-type mucosa has been shown to be related to the degree of esophageal acid exposure, the level of lower esophageal sphincter pressure and the length of the sphincter exposed to the abdominal pressure environment. It is now known that the segments of cardiac-type mucosa can show intestinal metaplasia on biopsy and that the prevalence of this finding is directly related to the length of the segment. On the bases of these studies, it is hypothesized that Barrett’s esophagus spreads progressively upwards in a stepwise fashion. Initially, short segments of inflamed cardiac-type mucosa develop below an endoscopically normal appearing gastroesophageal junction. The inflammation causes a loss in the pressure and length of the lower esophageal sphincter resulting in greater esophageal acid exposure with extension of inflamed cardiac-type mucosa into the distal 3 cm of the esophagus. With further loss of sphincter pressure and length, the process extends higher into the esophageal body. With time, and under proper conditions, intestinalization of the cardiac mucosa can occur with a prevalence that is related to the duration and functional severity of the disease. It is the occurrence of intestinalization that is associated with a cancer risk and is required for the diagnosis of Barrett’s esophagus. Understanding the disease in this way has strong implications regarding its therapy. Based on the above, the goals in the management of Barrett’s esophagus are as follows: (i) to prevent the development of the metaplastic epithelium by stopping reflux early in the disease process; (ii) to promote or induce healing or regression of the metaplastic epithelium such that the cancer risk mucosal change (intestinal metaplasia) is eliminated; and (iii) to induce a quiescence of the intestinalized metaplastic epithelium and halt its progression to dysplasia and cancer. The goal of therapy for Barrett’s esophagus according to the American College of Gastroenterology is to control the symptoms of gastroesophageal reflux disease . They state that symptom relief is an appropriate end-point for the therapy of Barrett s esophagus’. This approach has been shown to be ineffective, in that the eradication of symptoms cannot be equated with elimination of Address correspondence to: Dr T. R. DeMeester, 1510 San Pablo Street, Suite 514, Los Angeles, CA 90033-4612, USA. Tel: (323) 442 5925; Fax: (323) 442 5872; E-mail: [email protected] *Presented at the Meeting Standards and Controversies in the Treatment of Carcinoma of the Esophagus and Gastroesophageal Junction , Düsseldorf, Germany, Dec 2000. Meeting President: Professor Dr med B Ulrich, FACS, FRCS, Düsseldorf, Germany.