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When Norman Barrett described columnar metaplasia in the esophagus in 1950, he could not have predicted the controversies that would arise from the condition that now bears his name. In response to chronic injury from reflux esophagitis, the normally squamous-lined lower esophagus becomes reepithelialized with intestinal-type (mucus-secreting) columnar epithelium, giving rise to Barrett esophagus. In a minority of cases, this metaplastic epithelium develops dysplasia, which, in turn, can progress to esophageal adenocarcinoma, a malignant neoplasm associated with substantial morbidity and a 5-year survival rate of less than 20%. Over the past 40 years, the incidence of esophageal adenocarcinoma has risen markedly in the United States, from 0.4 cases per 100 000 in 1975 to 2.6 cases per 100 000 in 2009.1 Barrett esophagus and esophageal adenocarcinoma share similar epidemiologic risk factors, including gastroesophageal reflux disease (GERD), white race, male sex, increasing age, tobacco use, and central adiposity.
Lochhead P, Chan AT. Screening and Surveillance for Barrett Esophagus. JAMA Intern Med. 2015;175(2):159–160. doi:10.1001/jamainternmed.2014.6983
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