Barrett's esophagus (BE) is an acquired condition in which the squamous lining of the distal esophagus is replaced by a specialized intestinal metaplastic columnar epithelium. Although in the past BE was defined as the presence of columnar-lined esophagus on endoscopy, it is now accepted that confirmation of intestinal metaplasia by histology is required to make the diagnosis. The American College of Gastroenterology summarizes the most widely accepted definition as “a change in the esophageal epithelium of any length that can be recognized at endoscopy and is confirmed to have intestinal metaplasia by biopsy of the tubular esophagus and excludes intestinal metaplasia of the cardia.”1 The importance of BE is its risk of transforming into esophageal adenocarcinoma.
The incidence of BE over the past 20 years has risen sharply, and with it, there has been a dramatic increase in the incidence of adenocarcinoma.2 Reflux without BE can be treated medically (acid suppression) and surgically (fundoplication), with surgical therapy gaining increasing attention. Indeed, with the development of minimally invasive surgery, there has been an increased willingness to consider surgical options for reflux disease.3 From 1990 to 1997, the rate of antireflux surgery increased from 4.4 to 12.0 per 100,000 adults, and the proportion of operations performed laparoscopically increased from 25% to 76%.3 Similar trends have been noted in other countries as well.4,5 In this context, we review the available evidence for both medical and surgical approaches to the management of BE and their respective roles in halting disease progression.
The prevalence of BE in the population has been difficult to assess. Cameron and Lomboy at the Mayo Clinic found BE in 0.73% of 51,311 patients having endoscopy.6 In another endoscopy screening report, a prevalence rate of 1% was found in residents of Olmsted County, Minnesota.7 Still other studies have found much higher rates. Studies of patients undergoing screening sigmoidoscopy or colonoscopy who agreed to an upper endoscopy revealed BE in 10-25% of these patients.8–10 Seven cases were found in 733 autopsies (approximately 1%). The adjusted prevalence rate in this autopsy series was 376 cases per 100,000 population, significantly higher than the clinically diagnosed prevalence of 22.6 per 100,000.7,11 While many have suggested that the rate of BE has increased in the population, the incidence of BE has increased in parallel with the use of endoscopy.12,13 Whether there is a true increase in the incidence of BE or the increase simply reflects the increased use of endoscopy is unclear. In contrast, the incidence of esophageal adenocarcinoma has increased 10-fold in the 25-year period 1974–1997. Many adenocarcinomas occur in patients without a previous diagnosis of BE, suggesting that many people with this condition remain undiagnosed.13 The rate of malignant transformation of BE itself remains low. The overall risk of developing adenocarcinoma in patients with BE ranges from 0.2% to 1.9% per year.14