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Barrett's esophagus - Wikipedia, the free encyclopedia

Barrett's esophagus

From Wikipedia, the free encyclopedia

Barrett's esophagus
Classification and external resources
Endoscopic image of Barrett's esophagus, which is the area of red mucosa projecting like a tongue. Biopsies showed intestinal metaplasia.
ICD-10 K22.7
ICD-9 530.85
OMIM 109350
DiseasesDB 1246
MedlinePlus 001143
eMedicine radio/73 

Barrett's esophagus (sometimes called Barrett's syndrome, CELLO, columnar epithelium lined lower oesophagus 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 (19031979), Australian-born British surgeon at St Thomas' Hospital, who described the condition in 1957.[3]

Contents

[edit] Causes and Symptoms

Barrett's esophagus is caused by gastroesophageal reflux disease, GERD (UK: GORD), 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

[edit] Pathology

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.[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 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.

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.

[edit] 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. 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.[5]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.[6] Endoscopic mucosal resection (EMR) has also been evaluated as a management technique.[7]

Additionally an operation known as a Nissen fundoplication can reduce the reflux of acid from the stomach into the esophagus.[8]

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.[9][10] 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.

[edit] References

  1. ^ Stein H, Siewert J (1993). "Barrett's esophagus: pathogenesis, epidemiology, functional abnormalities, malignant degeneration, and surgical management". Dysphagia 8 (3): 276-88. doi:10.1007/BF01354551. 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. doi:10.1002/jso.20359. 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. ^ Overholt BF, Wang KK, Burdick JS, et al. (2007). "Five-year efficacy and safety of photodynamic therapy with Photofrin in Barrett's high-grade dysplasia.". Gastrointestinal endoscopy 66 (3): 460-8. PMID 17643436. 
  6. ^ Galipeau P, Li X, Blount PL, Maley CC, Sanchez CA Odze RD, Ayub K, Rabinovitch PS, Vaughan TV, Reid BJ (2007). "NSAIDs modulate CDKN2A, TP53, and DNA content risk for progression to esophageal adenocarcinoma" 4 (2): e67. PMID 17326708. 
  7. ^ Reshamwala P, Darwin P (2006). "Endoscopic management of early gastric cancer". Curr Opin Gastroenterol 22 (5): 541-5. doi:10.1097/01.mog.0000239870.04457.80. PMID 16891887. 
  8. ^ Abbas A, Deschamps C, Cassivi SD, et al. (2004). "The role of laparoscopic fundoplication in Barrett’s esophagus". Annals of Thoracic Surgery 77 (2): 393-396. doi:10.1016/S0003-4975(03)01352-3. PMID 14759403. 
  9. ^ Corley DA, Kerlikowske K, Verma R, Buffler P (2003). "Protective association of aspirin/NSAIDs and esophageal cancer: a systematic review and meta-analysis.". Gastroenterology 124: 47-56. doi:10.1053/gast.2003.50008. PMID 12512029. 
  10. ^ Vaughan TL, Dong LM, Blount PL, Ayub K, Odze RD, Sanchez, CA, Rabinovitch PS, Reid BJ (2005). "Non-steroidal anti-inflammatory drugs and risk of neoplastic progression in Barrett's oesophagus: a prospective study". Lancet Oncol 6: 945-52. doi:10.1016/S1470-2045(05)70431-9. PMID 16321762. 

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