A new review article covers the epidemiology, pathogenesis, and natural history of Barrett’s esophagus and management options for the disorder.
It has been estimated that 5.6% of adults in the United States have Barrett’s esophagus, the condition in which a metaplastic columnar mucosa that confers a predisposition to cancer replaces an esophageal squamous mucosa damaged by gastroesophageal reflux disease (GERD). GERD and Barrett’s esophagus are major risk factors for esophageal adenocarcinoma, a deadly tumor whose frequency in the United States has increased by a factor of more than 7 during the past four decades. The metaplastic columnar mucosa of Barrett’s esophagus causes no symptoms, and the condition has clinical importance only because it confers a predisposition to cancer.
• How is the diagnosis of Barrett’s esophagus made?
The diagnosis of Barrett’s esophagus requires findings on endoscopy that columnar mucosa extends above the gastroesophageal junction, lining the distal esophagus, plus esophageal-biopsy results that confirm the presence of columnar metaplasia. Endoscopically, the gastroesophageal junction is identified as the most proximal extent of gastric folds, and the columnar mucosa is salmon-colored and coarse, in contrast to the pale, glossy esophageal squamous mucosa.
The extent of esophageal columnar metaplasia determines whether long-segment or short-segment Barrett’s esophagus (greater than or equal to 3 cm or <3 cm of columnar metaplasia, respectively) is diagnosed. However, authorities disagree on the histologic type of columnar mucosa that establishes a diagnosis of Barrett’s esophagus. U.S. gastroenterology societies require esophageal biopsies showing intestinal metaplasia with goblet cells (also called specialized intestinal metaplasia or specialized columnar epithelium) for a definitive diagnosis of Barrett’s esophagus. This intestinal metaplasia is a well-established risk factor for adenocarcinoma.
• What are risk factors for Barrett’s esophagus as well as factors that may be protective?
Barrett’s esophagus is two to three times as common in men as in women, is uncommon in blacks and Asians, and is rare in children. Other important risk factors include obesity (with a predominantly intraabdominal fat distribution) and cigarette smoking, and there is a familial form of Barrett’s esophagus, which accounts for 7 to 11% of all cases. Most conditions associated with Barrett’s metaplasia are also risk factors for esophageal adenocarcinoma. Conversely, factors that might provide protection against Barrett’s esophagus include the use of nonsteroidal antiinflammatory drugs, gastric infection with Helicobacter pylori, and consumption of a diet high in fruits and vegetables.
Morning Report Questions
Q: What is the risk of esophageal adenocarcinoma in patients with nondysplastic Barrett’s esophagus?
A: Recent studies suggest that the risk of esophageal adenocarcinoma in the general population of patients with nondysplastic Barrett’s esophagus is only 0.1 to 0.3% per year. However, a number of factors influence the risk of cancer for individual patients. For example, cancer risk among men with Barrett’s esophagus is approximately twice that among women, the risk is greater with a longer segment of Barrett’s metaplasia, and the risk is especially high among persons with certain familial forms of Barrett’s esophagus. In addition, the risk appears to decrease with follow-up endoscopies showing no progression to dysplasia.
Q: How should Barrett’s esophagus be treated?
A: GERD should be treated aggressively in patients with Barrett’s esophagus, and there is indirect evidence to suggest that proton-pump inhibitors (PPIs) decrease the risk of cancer development. For example, a recent cohort study involving 540 patients with Barrett’s esophagus who were followed for a median of 5.2 years showed that PPI use was associated with a 75% reduction in the risk of neoplastic progression. Bile acids can also cause double-strand DNA breaks and might contribute to carcinogenesis in patients with Barrett’s metaplasia, and PPIs do not prevent bile reflux. Antireflux surgery can prevent reflux of all gastric contents (acid and bile), but the best available data suggest that surgery is not more effective than PPI therapy in preventing cancer. Thus, antireflux surgery is not advised solely for protection against cancer. Randomized, controlled trials have shown that endoscopic eradication of dysplasia in patients with Barrett’s esophagus with the use of photodynamic therapy or radiofrequency ablation (in which radiofrequency energy destroys the mucosa) significantly reduces the rate of progression to cancer. However, the efficacy of radiofrequency ablation for preventing cancer in patients with nondysplastic Barrett’s esophagus has not been established in long-term studies.