|Other names||Barrett's oesophagus, Allison-Johnstone anomaly, columnar epithelium lined lower oesophagus (CELLO)|
|Endoscopic image of Barrett's esophagus, which is the area of dark reddish-brown mucosa at the base of the esophagus.|
|Specialty||Gastroenterology, general surgery|
|Symptoms||Heartburn, acid reflux|
|Types||No dysplasia, low-grade dysplasia, high-grade dysplasia, invasive adenocarcinoma|
|Causes||Gastroesophageal reflux disease|
|Diagnostic method||Endoscopy, tissue biopsy|
|Differential diagnosis||Gastritis, esophageal spasm, Helicobacter pylori infection, gallstones, heart disease|
|Treatment||Surveillance, ablation, resection|
|Medication||Proton pump inhibitor|
Barrett esophagus (BE) is an abnormal change of the cells lining the lower portion of the esophagus from squamous epithelium to columnar epithelium. Though it does not result in symptoms itself, associated symptoms may include heartburn, acid reflux, and trouble swallowing. It is precancerous condition in which less than 5% develop esophageal adenocarcinoma.
The underlying mechanism is thought to be adaptation to long term acid exposure due to gastroesophageal reflux disease (GERD). Some cases may also run in families. Risk factors include hiatal hernia, pregnancy, obesity, asthma, diabetes, and peptic ulcer disease. It is classified into four types: nondysplastic, low-grade dysplasia, high-grade dysplasia, and invasive adenocarcinoma. Testing for the condition is recommended in males who have symptoms for more than five years along with other risk factors. Diagnosis is confirmed by seeing the characteristic appearance on endoscopy and tissue biopsy.
Treatment is generally with a proton pump inhibitor with further efforts depending on the type. When no dysplasia is present surveillance is recommended every 3 to 5 years. For low-grade dysplasia surveillance every 6 to 12 months or endoscopic ablation is recommended. For high-grade dysplasia treatment is with resection of the involve mucosa followed by ablation. If the mucosa looks normal but the biopsy is concerning radiofrequency ablation is recommended. If cancer is present surgery may be recommended.
About 1.5% of the general population and 10% of people with GERD are effected. The average age at diagnosis is 55. Males are effected more often than females. The condition may have been initially described in 1879 by Heinrich Quinke and 1906 by Wilder Tileston. Further descriptions occurred in 1950 by the surgeon Norman Barrett, after who it is named.
Signs and symptoms
The change from normal to premalignant cells that indicate Barrett's esophagus does not cause any particular symptoms. Barrett's esophagus, however, is associated with these symptoms:
- frequent and longstanding heartburn
- trouble swallowing
- vomiting blood
- pain under the sternum where the esophagus meets the stomach
- unintentional weight loss because eating is painful
The risk of developing Barrett's esophagus is increased by central obesity (vs. peripheral obesity). The exact mechanism is unclear. The difference in distribution of fat among men (more central) and women (more peripheral) may explain the increased risk in males.
Barrett's esophagus occurs due to chronic inflammation. The principal cause of the chronic inflammation is gastroesophageal reflux disease, GERD (UK: GORD). In this disease, acidic stomach, bile, and small intestine and pancreatic contents cause damage to the cells of the lower esophagus. Recently, bile acids were shown to be able to induce intestinal differentiation, in gastroesophageal junction cells, through inhibition of the epidermal growth factor receptor (EGFR) and the protein kinase enzyme Akt.
This results in the eventual up-regulation of the p50 subunit of protein complex NF-κB (NFKB1), and ultimately activation of the homeobox gene CDX2, which is responsible for the expression of intestinal enzymes such as guanylate cyclase 2C.
This mechanism also explains the selection of HER2/neu (also called ERBB2) and the overexpressing (lineage-addicted) cancer cells during the process of carcinogenesis, and the efficacy of targeted therapy against the Her-2 receptor with trastuzumab (Herceptin) in the treatment of adenocarcinomas at the gastroesophageal junction.
Researchers are unable to predict who with heartburn will develop Barrett's esophagus. While no relationship exists between the severity of heartburn and the development of Barrett's esophagus, a relationship does exist between chronic heartburn and the development of Barrett's esophagus. Sometimes, people with Barrett's esophagus have no heartburn symptoms at all.
Some anecdotal evidence indicates those with the eating disorder bulimia are more likely to develop Barrett's esophagus because bulimia can cause severe acid reflux, and because purging also floods the esophagus with acid. However, a link between bulimia and Barrett's esophagus remains unproven.
Both macroscopic (from endoscopy) and microscopic positive findings are required to make a diagnosis. 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.
Screening endoscopy is recommended among males over the age of 60 who have reflux symptoms that are of long duration and not controllable with treatment. Among those not expected to live more than 5 years screening is not recommended.
The Seattle protocol is used commonly in endoscopy to obtain endoscopic biopsies for screening, taken every 1-2 cm from the gastroesophageal junction.
The presence of goblet cells, called intestinal metaplasia, is necessary to make a diagnosis of Barrett's esophagus. This frequently occurs in the presence of other metaplastic columnar cells, but only the presence of goblet cells is diagnostic. The metaplasia 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.
Many histologic mimics of Barrett's esophagus are known (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). 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 used to identify true intestinal-type metaplastic cells. The protein AGR2 is elevated in Barrett's esophagus and can be used as a biomarker for distinguishing Barrett epithelium from normal esophageal epithelium.
The presence of intestinal metaplasia in Barrett's esophagus represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in Barrett's esophagus. Also intestinal metaplastic cells can be positive for CK 7+/CK20-.
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 epithelial dysplasia (or "intraepithelial neoplasia"). Among all metaplastic lesions, around 8% were associated with dysplasia. particularly a recent study demonstrated that dysplastic lesions were located mainly in the posterior wall of the Oesophagus.
Considerable variability is seen in assessment for dysplasia among pathologists. Recently, gastroenterology and GI pathology societies have recommended that any diagnosis of high-grade dysplasia in Barrett be confirmed by at least two fellowship-trained GI pathologists prior to definitive treatment for patients. For more accuracy and reproductibility, it is also recommended to follow international classification system as the "Vienna classification" of gastrointestinal epithelial neoplasia (2000).
Many people with Barrett's esophagus do not have dysplasia. Medical societies recommend that if a patient has Barrett's esophagus, and if the past two endoscopy and biopsy examinations have confirmed the absence of dysplasia, then the patient should not have another endoscopy within three years.
Endoscopic surveillance of people with Barrett's esophagus is often recommended, although little direct evidence supports this practice. Treatment options for high-grade dysplasia include surgical removal of the esophaguses (esophagectomy) or endoscopic treatments such as endoscopic mucosal resection or ablation (destruction).
The risk of malignancy is highest in the United States in Caucasian men over fifty years of age with more than five years of symptoms. Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes). Although in the past physicians have taken a watchful waiting approach, newly published research supports consideration of intervention for Barrett's esophagus. Balloon-based radiofrequency ablation, invented by Ganz, Stern, and Zelickson in 1999, is a new treatment modality for the treatment of Barrett's esophagus and dysplasia, and has been the subject of numerous published clinical trials. The findings demonstrate radiofrequency ablation has an efficacy of 90% or greater with respect to complete clearance of Barrett's esophagus and dysplasia with durability up to five years and a favorable safety profile.
Anti-reflux surgery has not been proven to prevent esophageal cancer. However, the indication is that proton pump inhibitors are effective in limiting the progression of esophageal cancer. Laser treatment is used in severe dysplasia, while overt malignancy may require surgery, radiation therapy, or systemic chemotherapy. A recent five-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.
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 the detection of three different genetic abnormalities was associated with as much as a 79% chance of developing cancer in six years.
Endoscopic mucosal resection has also been evaluated as a management technique. Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.
In a variety of studies, nonsteroidal anti-inflammatory drugs (NSAIDS), like aspirin, have shown evidence of preventing esophageal cancer in people with Barrett's esophagus. 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.
Barrett's esophagus is a precancerous condition, not a cancer itself. Its malignant sequela, esophagogastric junctional adenocarcinoma, has a mortality rate of over 85%. The risk of developing esophageal adenocarcinoma in people who have Barrett's esophagus has been estimated to be 6–7 per 1000 person-years, but a cohort study of 11,028 patients from Denmark published in 2011 showed an incidence of only 1.2 per 1000 person-years (5.1 per 1000 person-years in patients with dysplasia, 1.0 per 1000 person-years in patients without dysplasia).
The relative risk of esophageal adenocarcinoma is approximately 10 in those with Barrett's esophagus, compared to the general population. Most people with esophageal carcinoma survive less than one year. Rates of esophageal adenocarcinoma have increased in the Western world.
The incidence in the United States among Caucasian men is eight times the rate among Caucasian women and five times greater than African American men. Overall, the male to female ratio of Barrett's esophagus is 10:1. Several studies have estimated the prevalence of Barrett's esophagus in the general population to be 1.3% to 1.6% in two European populations (Italian and Swedish), and 3.6% in a Korean population.
The condition is named after Australian thoracic surgeon Norman Barrett (1903–1979), who in 1950 argued that ′ulcers are found below the squamocolumnar junction ... represent gastric ulcers within “a pouch of stomach … drawn up by scar tissue into the mediastinum” ... representing an example of a “congenital short esophagus”′. In contrast, Philip Rowland Allison and Alan Johnstone argued that the condition related to the ″esophagus lined with gastric mucous membrane and not intra-thoracic stomach as Barrett mistakenly believed.″ Philip Allison, cardiothoracic surgeon and Chair of Surgery at the University of Oxford, suggested ″calling the chronic peptic ulcer crater of the esophagus a “Barrett’s ulcer″, but added this name did not imply agreement with ″Barrett’s description of an esophagus lined with gastric mucous membrane as stomach.”
A further association was made with adenocarcinoma in 1975.
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