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Barrett esophagus (BE) is a condition in which the stratified squamous epithelium of the esophagus is replaced by intestinal columnar epithelium, a process called intestinal metaplasia (IM). Dr. Norman Barrett, an Australian thoracic surgeon, characterized the findings in an article that he published in 1950.1 In 1953, the association was made between BE and gastroesophageal reflux disease (GERD) by the English thoracic surgeon Dr. Philip Allison.2 The etiology of BE is accepted to be due to chronic exposure of the esophageal epithelium to gastroduodenal refluxate. The importance of BE is its potential to progress and develop into adenocarcinoma. The association between BE and esophageal adenocarcinoma was established in a case report in 1975 by Dr. Alan Farnsworth, a cardiac surgeon, in which he identified adenocarcinoma in a segment of BE.3

Multiple factors have been identified that lead to an increased risk of developing BE. These include age over 50 years, male gender, white race, elevated body mass index (BMI), intra-abdominal distribution of body fat, hiatal hernia, and chronic GERD.4 BE is diagnosed by endoscopic biopsy and histologic examination which identifies the IM (Fig. 41-1).

Figure 41-1

Barrett esophagus: EGD and histology.

Progression of BE to cancer is recognized as a continuum through dysplasia to cancer. As such, the histologic examination of this disease is often classified into BE without dysplasia, BE with low-grade dysplasia (LGD), and BE with high-grade dysplasia (HGD). Progressive severity of dysplasia leads to a higher risk for the development of esophageal cancer. BE without dysplasia has a 0.5% per year risk of developing into esophageal cancer, whereas BE with LGD has a 1.4% per year risk and BE with HGD has a 6% per year risk.5 It is this strong association between BE and esophageal adenocarcinoma that has driven the aggressive surveillance and treatment of BE.


The goal of surveillance is to reduce mortality of a disease by early diagnosis. In the case of BE, the goal of surveillance is to reduce the mortality due to esophageal cancer. The risk of developing esophageal cancer in the general Western population is low; therefore, routine endoscopic screening has not been recommended. For patients who have risk factors for BE as described earlier, there is some data supporting screening endoscopy. Therefore, the American College of Gastroenterology recommends that screening endoscopy in this patient population should be individualized.6

For patients already diagnosed with BE, it is a common practice to perform endoscopic surveillance to search for signs of progression to cancer. Although this makes intuitive sense, there is a lack of randomized clinical trials to identify the true effectiveness of endoscopic surveillance in patients with BE. There have, however, been population studies that have shown the practice to lead to earlier detection ...

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