Short segment Barrett’s esophagus is an increasing concern in the management of chronic gastroesophageal reflux. Traditionally, the diagnosis of Barrett’s esophagus has been made by endoscopic evidence of a columnar epithelial-lined esophagus extending more than 3 cm above the gastroesophageal junction in conjunction with histopathologic findings of intestinal metaplasia on endoscopic biopsy specimens. However, the geographic criterion for this classic form of Barrett’s esophagus, also known as long-segment Barrett’s esophagus, is arbitrary and should be recognized as such.
The present study sought to determine whether short segments of specialized intestinal epithelium can occur in the distal esophagus and, if so, are premalignant. In 20 patients with reflux symptoms and endoscopic evidence of Barrett’s esophagus, the length of the affected mucosa was determined by endoscopy. Histopathologic analysis of the mucosa was performed for low- and high-grade dysplasia.
Barrett’s esophagus develops as a consequence of chronic gastroesophageal reflux. The underlying mucosal abnormality is an abnormal proliferation of intestinal epithelial cells. The progression of these cells to esophageal adenocarcinoma is usually slow and gradual, with cellular changes occurring from within the mucosal column, rather than at the point of contact with esophageal stroma.
To date, it has been reported that a small fraction of patients with distal Barrett’s esophagus have short segments of the disease. These segments typically consist of a few fingerlike projections of the abnormal epithelium. The term “short segment Barrett’s esophagus” is used to distinguish this variant from long-segment Barrett’s because it is less likely to progress to esophageal cancer.
In addition to the morphologic characteristics of the Barrett’s mucosa, a number of radiographic features can be identified on double-contrast esophagography that are characteristic of long-segment Barrett’s, such as reflux esophagitis and peptic scarring of the esophagus and a distinctive reticular pattern in the mid esophagus [1].
Although it is thought that short-segment Barrett’s carries a lower risk for progression to esophageal adenocarcinoma than does long-segment disease, this conclusion should be viewed cautiously. Until further studies are undertaken, it is recommended that all patients with Barrett’s esophagus be placed on surveillance, even those with short-segment disease. In the future, it is possible that the development of a new endoscopic treatment for Barrett’s esophagus, such as ablation therapy using proton pump inhibition or photodynamic therapy combined with acid suppression, might allow some patients to be followed without needing surveillance. This technique would work by injuring the epithelial cells of Barrett’s esophagus and then treating it in a reduced-acid environment, thus potentially converting it to normal squamous mucosa. These techniques are currently under development. If successful, they may enable more patients to be followed without surveillance, and thereby decrease the incidence of esophageal cancer related to recurrent acid exposure. Such a strategy should be considered as soon as the technology becomes available.
