Barrett's esophagus
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Barrett's esophagus refers to an abnormal change (metaplasia) in the cells of the lower end of the esophagus thought to be caused by damage from chronic acid exposure, or reflux esophagitis. Barrett's esophagus is found in about 10% of patients who seek medical care for heartburn (gastroesophageal reflux). It is considered to be a premalignant condition and is associated with an increased risk of esophageal cancer.
The condition is named after Dr Norman Barrett (1903-1979), Australian-born British surgeon at St Thomas' Hospital, who described the condition in 1957.
Treatment
Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes) every 12 months or so whilst the underlying reflux is controlled with H2 antagonists or proton pump inhibitor drugs in combination with measures to prevent reflux. In severe dysplasia, laser treatment is being used, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. There is presently no reliable way to determine which patients with Barrett's esophagus will go on to develop esophageal cancer.
Pathology
Barrett's esophagus is marked by the presence of columnar cell epithelium in the lower esophagus, replacing the normal squamous cell epithelium—an example of metaplasia. The columnar epithelium is better able to withstand the erosive action of the gastric secretions; however, this metaplasia confers an increased cancer risk of the adenocarcinoma type.
The metaplastic columnar cells may be of two types: gastric (similar to those in the stomach) or colonic (similar to cells in the intestines). A biopsy of the affected area will often contain a mixture of the two. Colonic-type metaplasia confers a higher risk of malignancy.
The metaplasia of Barrett's esophagus is visible grossly through a gastroscope, but biopsy specimens must be examined under a microscope to determine whether cells are gastric or colonic in nature.
Reference
- Barrett NR. The lower esophagus lined by columnar epithelium. Surgery 1957;41:881-894. PMID 13442856.