In Barrett esophagus, healthy esophageal epithelium is replaced with metaplastic columnar cells—the result, it is believed, of damage from prolonged exposure of the esophagus to the refluxate of gastroesophageal reflux disease (GERD). The inherent risk of progression from Barrett esophagus to adenocarcinoma of the esophagus has been established.
Signs and symptoms
The classic picture of a patient with Barrett esophagus is a middle-aged (55 yr) white man with a chronic history of gastroesophageal reflux—for example, pyrosis, acid regurgitation, and, occasionally, dysphagia. Some patients, however, deny having any symptoms.
The features of GERD in relation to long-segment Barrett esophagus (LSBE, >3 cm) and short-segment Barrett esophagus (SSBE, 5 yr), particularly those aged 50 years or older, have an upper endoscopy to detect or screen for Barrett esophagus.
See Workup for more detail.
Once Barrett esophagus has been identified, patients should undergo periodic surveillance endoscopy to identify histologic markers for increased cancer risk (dysplasia) or cancer that is at an earlier stage and is amenable to therapy. Dysplasia is the best histologic marker for cancer risk.
The management options for high-grade dysplasia include the following:
Surveillance endoscopy, with intensive biopsy at 3-month intervals until cancer is detected
Endoscopic ablation: In most major medical centers, ablation is first-line therapy
Surgical resection: While studies have shown surgery to be efficacious in the control of GERD symptoms, no good evidence indicates that surgical therapy provides regression in Barrett esophagus
Pharmacologic treatment for Barrett esophagus should be the same as that for GERD, although most authorities agree that treatment should employ a proton pump inhibitor (PPI) instead of an H2-receptor antagonist, due to the relative acid insensitivity of patients with Barrett esophagus. While PPIs have been found to be better than H2-receptor antagonists at reducing gastric acid secretion, the evidence as to whether PPIs induce regression of Barrett esophagus remains inconclusive.
The diet for patients with Barrett esophagus is the same as that recommended for patients with GERD. Patients should avoid the following:
Fried or fatty foods
Citrus fruits or juices
Aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs)
See Treatment and Medication for more detail.
Barrett esophagus is well recognized as a complication of gastroesophageal reflux disease (GERD). Prolonged exposure of the esophagus to the refluxate of GERD can erode the esophageal mucosa, promote inflammatory cell infiltrate, and ultimately cause epithelial necrosis. This chronic damage is believed to promote the replacement of healthy esophageal epithelium with the metaplastic columnar cells of Barrett esophagus. Why only some people with GERD develop Barrett esophagus is not clear (see the image below).
The definition of Barrett esophagus (BE) has evolved considerably over the past 100 years. In 1906, Tileston, a pathologist, described several patients with “peptic ulcer of the oesophagus” in which the epithelium around the ulcer closely resembled that normally found in the stomach. The debate for the next 4 decades centered on the anatomic origin of this mucosal anomaly. Many investigators, including Barrett in his treatise published in 1950, supported the view that this ulcerated, columnar-lined organ was, in fact, the stomach tethered within the chest by a congenitally short esophagus. 
In 1953, Allison and Johnstone argued that the columnar organ was more likely esophagus, because the intrathoracic region lacked a peritoneal covering, contained submucosal glands and muscularis propria characteristic of the esophagus, and could harbor islands of squamous cells within the columnar segment.  In 1957, Barrett agreed and suggested that the condition that bears his name be referred to as “lower esophagus lined by columnar epithelium.”  For the next 2 decades, descriptions of the histology of Barrett esophagus varied considerably from acid-secreting, fundic-type epithelium to intestinal-type epithelium with goblet cells.
Finally, in 1976, Paull et al published a report on the histologic spectrum of Barrett esophagus in which they used manometric guidance for their biopsies.  The study’s patients had 1 or a combination of 3 types of columnar epithelium; ie, a gastric fundic-type, a junctional type, and a distinctive type of intestinal metaplasia the investigators called “specialized columnar epithelium.” This specialized intestinal metaplasia (SIM), complete with goblet cells, has become the sine qua non for the diagnosis of Barrett esophagus.
However, while Paull et al’s study clarified the nature of the histologic lesion, the endoscopic definition of Barrett esophagus has continued to change. Many people believed that the distal esophagus could contain a normal region of columnar mucosa. In addition, determining the exact location of the esophagogastric junction (EGJ) in patients with Barrett esophagus often is difficult. To avoid false-positive diagnoses, investigators selected arbitrary lengths of columnar-lined esophagus to establish a diagnosis for their studies. Eventually, community endoscopists embraced this practice, and biopsy of the so-called normal distal columnar-lined esophagus was avoided.
Convincing evidence indicates that SIM, the hallmark histologic lesion of Barrett esophagus, predisposes to dysplasia and cancer regardless of the endoscopic location. Thus, the definition of Barrett esophagus currently is the finding of SIM anywhere within the tubular esophagus.