Video: Dr. Jonathan Cohen of the Concorde Medical Group discusses Barrett's Esophagus Barrett's esophagus (sometimes called Barrett's syndrome, CELLO, columnar epithelium lined lower (o)esophagus or colloquially 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] 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.[2] The condition is named after Dr. Norman Barrett, Australian-born British surgeon at St Thomas' Hospital, who described the condition in 1957.[3]
Causes and Symptoms Barrett's esophagus is caused by gastroesophageal reflux disease, which allows the stomach's contents to damage the cells lining the lower esophagus. However, not every person who has GERD will develop Barrett's 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 Barrett's esophagus is marked by the presence of columnar epithelia in the lower esophagus, replacing the normal squamous cell epithelium-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.[4] 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 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. 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 occuring 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.
In the United States, it is estimated that 8 - 12% of patients who are diagnosed with Barrett's esophagus have been mis-diagnosed. This significant diagnostic error may result in higher rates of medical and life insurance rates for those mis-diagnosed; as well as enrollment of patients in unnecessary surveillance programs (i.e. annual endoscopic evaluation and biopsy to monitor for the development of Barrett's esophagus).
Second (consulting) opinions on pathologic materials are easily available as slides and tissue blocks are retained for 10 and 20 years, respectively. To request a consultation opinion, patients may contact their gastroenterologist for referral to a GI pathology specialty center. 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. Recent evidence has pointed to a similar condition developing in the distal gut epithelium. Barrett's Anus is a metaplastic change in the distal rectum whose cellularity is similar to that of the gastric mucosa.
While the condition is stable for many years, there has been recent evidence to show that it is the predisposing lesion to both anal teratoma and squamous cell carcinoma of the anus. Frequent bouts of steatorrhea are commonly cited as the most likely cause of Barrett's Anus, but much more research needs to be done in order to rule out causes such as HPV 8,13.
Treatment Current recommendations include routine endoscopy and biopsy (looking for dysplastic changes) every 12 months or so while the underlying reflux is controlled with proton pump inhibitor drugs in combination with measures to prevent reflux. laser treatment is used in severe dysplasia, 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. Endoscopic mucosal resection (EMR) has also been evaluated as a management technique.[5] Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.[6] References 1.^ Stein H, Siewert J (1993). "Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management".
Dysphagia 8 (3): 276-88. PMID 8359051. 2.^ Koppert L, Wijnhoven B, van Dekken H, Tilanus H, Dinjens W (2005). "The molecular biology of esophageal adenocarcinoma". J Surg Oncol 92 (3): 169-90. PMID 16299787. 3.^ Barrett N (1957). "The lower esophagus lined by columnar epithelium". Surgery 41 (6): 881-94. PMID 13442856. 4.^ Fléjou J (2005).
"Barrett's oesophagus: from metaplasia to dysplasia and cancer". Gut 54 Suppl 1: i6-12. PMID 15711008. 5.^ Reshamwala P, Darwin P (2006). "Endoscopic management of early gastric cancer". Curr Opin Gastroenterol 22 (5): 541-5. PMID 16891887. 6.^ Abbas A, Deschamps C, Cassivi SD, et al. (2004). "The role of laparoscopic fundoplication in Barrett%u2019s esophagus".
Annals of Thoracic Surgery 77 (2): 393-396. PMID 14759403. Source: Wikipedia (as of November 8, 2007) Copyright (c) Empowered Media 2007 Permission is granted to copy, distribute and/or modify this document under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation; with no Invariant Sections, no Front-Cover Texts, and no Back-Cover Texts. A copy of the license is included in the section entitled "GNU Free Documentation License".