Am Fam Physician. 2004 May 1;69(9):2061-2063.
In Barrett’s esophagus, the normal squamous lining of the distal esophagus is replaced with a metaplastic, intestinal, columnar epithelium. Barrett’s esophagus represents the end stage of severe, uncontrolled gastroesophageal reflux disease (GERD). However, Barrett’s esophagus also is recognized as a precursor for most cases of esophageal adenocarcinoma.1
With the recent increase in the incidence of esophageal adenocarcinoma and its association with GERD, endoscopic screening for Barrett’s esophagus has been suggested in the hope of decreasing the morbidity and mortality associated with this cancer, as described by Shalauta and Saad2 in this issue of American Family Physician. While the risk of developing esophageal cancer is relatively small in the general population, the risk for a person with Barrett’s esophagus is much greater.
The literature allows us to make the following assumptions with some degree of certainty: (1) 10 to 20 percent of adults in the United States have reflux; (2) about 10 percent of patients with reflux have Barrett’s esophagus; and (3) about 5 to 10 percent of patients with Barrett’s esophagus eventually develop cancer. Given these suppositions, the pool of patients requiring surveillance endoscopy and biopsy for Barrett’s esophagus may range from 0.5 to 2 percent of the adult population.3
The diagnosis of Barrett’s esophagus requires systematic biopsy of esophageal mucosa with abnormal appearance to detect the presence of specialized intestinal metaplasia. Endoscopy should not be performed for this indication without the ability and intent to obtain appropriate histologic samples of lesions. All areas that are abnormal in appearance should be sampled, and longer segments of Barrett’s esophagus should be biopsied every 2 cm.
The routine biopsy of a squamocolumnar junction of normal appearance should be discouraged because intestinal metaplasia not within the esophagus does not seem to have the same premalignant potential.4 The endoscopist must carefully document the location of the biopsies and clearly communicate this information to the pathologist.
Which patients with GERD should have upper endoscopy? Heartburn and regurgitation are fairly specific symptoms of GERD, and most patients with GERD can be managed empirically without endoscopy. Endoscopy is indicated to evaluate the so-called alarm symptoms (i.e., dysphagia, odynophagia, bleeding, and weight loss) and to screen for Barrett’s esophagus.5 The epidemiology of Barrett’s esophagus is not completely understood, but the risk seems to be higher in patients with long-term symptoms, especially white men. Some researchers have suggested a one-time screening endoscopy in all patients with chronic GERD, while others have limited this screening recommendation to patients older than 40 to 50 years who have had GERD symptoms for at least five years. All authorities would prefer long-term, evidence-based data on which to base clinical recommendations; however, these data will not be available for many years.
Currently, clinical practice should be based on the imperfect data that are available. The original American College of Gastroenterology Practice Guidelines of the Diagnosis Surveillance and Therapy of Barrett’s Esophagus6 recommended that patients with longstanding GERD symptoms, particularly patients 50 years or older, have upper endoscopy to detect Barrett’s esophagus. The more recent guideline was a bit more vague but continued to advocate for screening endoscopy in patients with chronic GERD symptoms.7
Where does this leave us when trying to determine which patients to screen for Barrett’s esophagus? A patient younger than 40 years with mild, infrequent symptoms may be managed without endoscopy. We must remember that we have no data showing that symptom-driven treatment prevents the development of Barrett’s esophagus and, therefore, even these patients eventually may require screening as they age and their duration of acid exposure increases. Most patients with heartburn who are older than 40 to 50 years have chronic symptoms, and it is not unreasonable to screen them (especially white men), regardless of the severity of their symptoms. Patients who initially present with chronic symptoms (i.e., more than five years) and those who have been followed for several years with reflux symptoms might be included in this group.
Furthermore, patients older than 65 years with new-onset GERD symptoms probably should have early endoscopy because their symptoms are less specific and mucosal disease often is more severe in this age group.8 Finally, there is no need to withhold therapy while waiting for endoscopy. Although not proved in clinical trials, treating a patient before endoscopy is performed may increase the ability of the endoscopist to recognize Barrett’s esophagus and may decrease the risk of a biopsy showing false dysplasia that is actually caused by acid-induced inflammation.
Aggressive use of endoscopy would mean that most patients with GERD would be scoped eventually, which would put economic pressure on the health care system. We can help in limiting the cost of this approach by avoiding inappropriate repeated screening in patients who have already had negative endoscopy results. Most clinicians think that once Barrett’s esophagus has been excluded with a single endoscopy, the risk of that patient subsequently developing Barrett’s esophagus is low enough to exclude further screening (probably in the patient’s lifetime). Adhering to current guidelines that have expanded the screening interval for nondysplastic Barrett’s esophagus to three years also is important.6 The cost savings from appropriate use of surveillance would help to offset the cost of screening a larger segment of the population, just as has been advocated in colon cancer screening.
Kenneth R. DeVault, M.D., is professor of medicine at Mayo Clinic Jacksonville, Jacksonville, Fla.
Address correspondence to Kenneth R. DeVault, M.D., Mayo Clinic Jacksonville, 4300 San Pablo Rd., Jacksonville, FL 32224. Reprints are not available from the author.
1. Spechler SJ, Goyal RK. The columnar-lined esophagus, intestinal metaplasia, and Norman Barrett. Gastroenterology. 1996;110:614–21.
2. Shalauta MD, Saad R. Barrett’s esophagus. Am Fam Physician. 2004;69:2113–8.
3. DeVault KR. Epidemiology and significance of Barrett’s esophagus. Dig Dis. 2000–2001;18:195–202.
4. Sharma P, Weston AP, Morales T, Topalovski M, Mayo MS, Sampliner RE. Relative risk of dysplasia for patients with intestinal metaplasia in the distal oesophagus and in the gastric cardia. Gut. 2000;46:9–13.
5. DeVault KR, Castell DO. Updated guidelines for the diagnosis and treatment of gastroesophageal reflux disease. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol. 1999;94:1434–42.
6. Sampliner RE. Practice guidelines on the diagnosis, surveillance and therapy of Barrett’s esophagus. The Practice Parameters Committee of the American College of Gastroenterology. Am J Gastroenterol. 1998;93:1028–32.
7. Sampliner RE, for the Practice Parameters Committee of the American College of Gastroenterology. Updated guidelines for the diagnosis, surveillance, and therapy of Barrett’s esophagus. Am J Gastroenterol. 2002;97:1888–95.
8. Richter JE. Gastroesophageal reflux disease in the older patient: presentation, treatment, and complications. Am J Gastroenterol. 2000;95:368–73.
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