BARRETT ESOPHAGUS
The current definition of Barrett esophagus is very different from the original definition proposed by Dr. Norman Barrett. Barrett esophagus is presently defined by the presence of metaplastic tissue in the distal esophagus resulting from chronic gastroesophageal reflux. The etiology of Barrett esophagus is primarily gastroesophageal reflux, but other important risk factors are involved. For example, Barrett esophagus occurs predominantly in white men. This may in part reflect a genetic predisposition but also an increased incidence of central obesity in white men. Cigarette smoking is also a likely cofactor, and Helicobacter pylori infection is protective.
Defining the presence of Barrett
esophagus is unfortunately easier said than done for two reasons: (1) There is
no clear definition of the endoscopic appearance of a normal squamocolumnar
junction and, therefore, of what defines a clear demarcation between the
esophagus and the proximal stomach. This is problematic because nearly 20% of
normal adults have metaplastic tissue in the gastric cardia adjoining the
distal esophagus, leading to confusion when a putative esophageal biopsy is
taken errantly from the gastric side. As a result, many patients are mislabeled
as having Barrett esophagus from biopsies taken incidentally from the gastric
cardia. (2) It is primarily the intestinalized metaplastic tissue that carries
the premalignant potential of Barrett esophagus. On the other hand, esophageal
metaplastic epithelium is commonly admixed with both cardiac and intestinal
metaplasia, making the finite sampling of endoscopic biopsies limited in
confirming the presence of extant intestinal metaplasia. As a result, the
British guidelines include both gastric and intestinalized epithelium in the
definition of Barrett esophagus. Diagnostic criteria thus vary amongst
gastrointestinal societies.
Endoscopically, the distal
esophagus is examined for the appearance of a salmoncolored mucosa, different
from the normal pinkwhite squamous mucosa, encroaching proximally at the
normal squamocolumnar junction. For the reason cited above, however, arbitrary
minimum lengths of this encroachment may be defined from 1 mm to 2 cm above the
gastroesophageal junction. Patients are
somewhat arbitrarily divided into those with longsegment disease (> 3 cm)
or shortsegment disease (< 3 cm). The Prague classification more
precisely categorizes the extent of the circumferential and maximal lengths of
grossly metaplastic epithelium.
There are two concerns with Barrett
esophagus. The first is that it represents a severe form of gastroesophageal
reflux with an associated risk of erosive esophagitis and stricture formation.
The second is that it has premalignant potential given the cellular instability
of metaplasia. Although the estimates of developing adenocarcinoma are low
(0.2% to 0.4% per year), they are derived from surveillance programs that miss
most prevalent forms of adenocarcinoma. Treatment consists of controlling the
reflux pharmacologically or surgically and asking the patient to participate in
endoscopic surveillance programs for potential detection of dysplasia and
cancer. For patients who develop dysplasia, there is also the evolving option
of radiofrequency ablation of the Barrett mucosa and/or endoscopic mucosal
resection to avoid de elopment of cancer and the need for esophagectomy.
