Barrett esophagus is a precancerous condition that
develops in up to 10% of patients who have of long-standing GERD. Most
of the patients with first diagnosis of Barrett esophagus are between
the ages of 40 and 60, although children can occasionally develop this
condition. The highest incidence is among white males. In addition to
the symptoms of gastroesophageal reflux disease, Barrett esophagus is
clinically significant due to the secondary complications of local
ulceration with bleeding and stricture. Barrett esophagus is the single
most important risk factor for the development of esophageal
adenocarcinoma; in fact patients diagnosed with Barrett’s disease have a
30-40 fold increase in risk. Adenocarcinoma of the esophagus is
associated with a very poor prognosis, with less than 20% over-all five
year survival.
The pathogenesis of Barrett Esophagus is unclear,
but it appears to result from an alteration in the differentiation
program of stem cells of the esophageal mucosa (5). The hallmark of
Barrett esophagus is columnar metaplasia; a process in which the distal
non-keratinized stratified squamous epithelium is replaced by
metaplastic columnar epithelium as a response to prolonged mucosal
injury. It is hypothesized that initially the metaplasia is a
protective process, allowing for the replacement of the acid damaged
esophageal epithelium by that of gastric epithelium. But like with any
process that involves increased mitosis there is an increased risk of
developing cancer.
