Barrett's esophagus (British English: oesophagus) (sometimes called Barrett's syndrome, CELLO,

columnar epithelium lined lower esophagus and colloquially referred to as Barrett's) 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.[1] The normal lining of the esophagus
(squamous epithelium) is replaced by an intestinal-type lining (columnar epithelium).
Barrett's esophagus is found in 5-15% of patients who seek medical care for heartburn
(gastroesophageal reflux disease, GERD), although a large subgroup of patients with Barrett's esophagus
do not have symptoms.[2] It is considered to be a premalignant condition because it is associated with an
increased risk of esophageal cancer (more specifically, adenocarcinoma) of about 0.5% per patient-year.
[3][2]
Diagnosis of Barrett's esophagus requires endoscopy (more specifically,
esophagogastroduodenoscopy, a procedure in which a small tube with a camera at the top is used to
look at the esophagus, stomach and first part of the bowels) and biopsy (taking small tissue samples
which are analysed using microscopy). The progression from Barrett's esophagus to esophageal cancer is
divided into non-dysplastic changes, low-grade and high-grade dysplasia (abnormal cell maturation
associated with a risk of progression to cancer) and frank carcinoma. In high-grade dysplasia, the risk of
developing cancer might be at 10% per patient-year or greater. [2]
Many professional medical societies propose endoscopic screening of patients with GERD and
endoscopic surveillance of patients with Barrett's esophagus, although little direct evidence supports
this practice, which is common in many developed countries. [2] Treatment options for high-grade
dysplasia include surgical removal of the esophagus (esophagectomy) or endoscopic treatments such as
endoscopic mucosal resection or ablation (destruction). Currently, there is no intervention that has been
shown to prevent the development of Barrett's esophagus or its progression to esophageal cancer. [2]
The condition is named after Norman Barrett (1903–1979) who described the condition in 1957.
Contents
 Causes and symptoms
 Pathology
 Treatment
 Additional images
 References
 External links
Causes and symptoms
Barrett's esophagus is caused by gastro-oesophageal reflux disease, GORD(USA: GERD), which
allows the stomach's contents to damage the cells lining the lower esophagus. Researchers are unable
to predict which heartburn sufferers will develop Barrett's esophagus. While there is no relationship
between the severity of heartburn and the development of Barrett's esophagus, there is a relationship
between chronic heartburn and the development of Barrett's esophagus. Sometimes people with
Barrett's esophagus will have no heartburn symptoms at all. In rare cases, damage to the esophagus
may be caused by swallowing a corrosive substance such as lye.
The change from normal to premalignant cells that indicates Barrett's esophagus does not cause
any particular symptoms. However, warning signs that should not be ignored include:
 frequent and longstanding heartburn
 trouble swallowing (dysphagia)
 vomiting blood
 pain under the breastbone where the esophagus meets the stomach
 unintentional weight loss because eating is painful
Pathology

Micrograph of Barrett's esophagus (left of image) and normal stratified squamous epithelium
(right of image). Alcian blue stain.

High magnification micrograph of Barrett's esophagus showing the characteristic goblet cells.
Alcian blue stain.
Barrett's esophagus is marked by the presence of columnar epithelia in the lower esophagus,
replacing the normal squamous cell epithelium—an example of metaplasia. The secretory columnar
epithelium may be more able to withstand the erosive action of the gastric secretions; however, this
metaplasia confers an increased risk of adenocarcinoma.
The metaplastic columnar cells may be of two types: gastric (similar to those in the stomach,
which is NOT technically Barrett's esophagus) 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 is the type of
metaplasia associated with risk of malignancy in genetically susceptible people.
The metaplasia of Barrett's esophagus is grossly visible through a gastroscope, but biopsy
specimens must be examined under a microscope to determine whether cells are gastric or colonic in
nature. Colonic metaplasia is usually identified by finding goblet cells in the epithelium and is necessary
for the true diagnosis of Barrett's.
There are many histologic mimics of Barrett's esophagus (i.e. goblet cells occurring in the
transitional epithelium of normal esophageal submucosal gland ducts, "pseudogoblet cells" in which
abundant foveolar (gastric) type mucin simulates the acid mucin true goblet cells). Assessment of
relationship to submucosal glands and transitional-type epithelium with examination of multiple levels
through the tissue may allow the pathologist to reliably distinguish between goblet cells of submucosal
gland ducts and true Barrett's esophagus (specialized columnar metaplasia). Use of the histochemical
stain Alcian blue pH 2.5 is also frequently used to distinguish true intestinal-type mucins from their
histologic mimics. Recently, immunohistochemical analysis with antibodies to CDX-2 (specific for mid
and hindgut intestinal derivation) has also been utilized to identify true intestinal-type metaplastic cells.
It has been shown that the protein AGR2 is elevated in Barrett's esophagus, [6] and can be used as a
biomarker for distinguishing Barrett's epithelium from normal esophageal epithelium. [7]
After the initial diagnosis of Barrett's esophagus is rendered, affected persons undergo annual
surveillance to detect changes that indicate higher risk to progression to cancer: development of
dysplasia. There is considerable variability in assessment for dysplasia among pathologists. Recently,
gastroenterology and GI pathology societies have recommended that any diagnosis of high grade
dysplasia in Barrett's be confirmed by at least two fellowship trained GI pathologists prior to definitive
treatment for patients
Treatment
The risk of malignancy is highest in the U.S. in Caucasian men > 50 years of age with > 5 years of
symptoms. It is unusual for African-American men to develop adenocarcinoma of the esophagus, the
cancer associated with Barrett's. Current recommendations include routine endoscopy and biopsy
(looking for dysplastic changes). If two endoscopies and biopsy sessions performed within 12 months
are negative for dysplasia then surveillance can be performed every 3 years while the underlying reflux
is controlled with proton pump inhibitor drugs in combination with measures to prevent reflux. For
patients found to have low grade or high grade dysplasia close observation and repeat endoscopy and
biopsies are indicated and the patient should be followed closely by a gastroenterologist.
Proton pump inhibitor drugs have not yet been proven to prevent esophageal cancer. Laser
treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or
systemic chemotherapy. Additionally, a recent 5-year random-controlled trial has shown that
photodynamic therapy using photofrin is statistically more effective in eliminating dysplastic growth
areas than sole use of a proton pump inhibitor. [8]There is presently no reliable way to determine which
patients with Barrett's esophagus will go on to develop esophageal cancer, although a recent study
found that the detection of three different genetic abnormalities were associated with as much as a 79%
chance of developing cancer in 6 years. [9]
Endoscopic mucosal resection (EMR) has also been evaluated as a management technique. [10]
Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the
stomach into the esophagus.[11]
In a variety of studies, non-steroidal anti-inflammatory drugs (NSAIDS), like aspirin, have shown
evidence of preventing esophageal cancer in Barrett's esophagus patients. [12][13] However, none of these
studies have been randomized, placebo controlled trials, which are considered the gold standard for
evaluating a medical intervention. In addition, the best dose of NSAIDs for cancer prevention is not yet
known.