Monday, March 12, 2012

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Barrett's esophagus

Barrett’s esophagus is characterized by an intestinal metaplastic change in the lining mucosa of the esophagus in response to chronic gastro­esophageal reflux. 
The condition is named after Norman Barrett, an Australian surgeon who drew attention to the columnar-lined esophagus in 1950.
It is still not well understood why some people develop esophagitis and others develop Barrett’s esophagus often without significant esophagitis. 

In Barrett’s esophagus the junction between squamous esophageal mucosa and gastric mucosa moves proximally. The columnar epithelium is more acid resistant than the squamous epithelium. So this metaplasia appears to be a protective adaptation. The patient of chronic reflux esophagitis will find his symptoms decrease when he has developed Barrett's esophagus.

It is mainly seen in white man and the prevalence increases with age. 
Several types of gastric-type mucosa may be found in the lower esophagus. When intestinal metaplasia occurs there is an increased risk of adenocarcinoma of the esophagus of the order of 25 times that of the general population. A recent (Dec 2011) large scale study in Denmark however shows that the incidence of adenocarcinoma in Barrett’s esopahgus is actually much lower i.e. around 7 times that of general population.

Clinical features:
The patient will have all the complaints of reflux esophagitis. Heartburn, described as a substernal burning sensation that moves from the region of the xiphoid up toward the neck. Regurgitation, water-brash and  odynophagia may be the other symptoms.

Barrett’s esophagus is diagnosed by endoscopic examination and  2  criteria  must  be  fulfilled.
1) The endoscopist must ascertain that columnar epithelium lines the distal esophagus.
2) Biopsy specimens of that columnar epithelium must show evidence of metaplasia.

To ascertain that columnar epithelium lines the distal esophagus, the endoscopist first must locate the esophagogastric junction (EGJ, which is recognized as the most proximal extent of the gastric folds) and then determine that columnar epithelium extends above the EGJ into the esophagus. Endoscopically, columnar epithelium has a reddish color and velvet-like texture that can be distinguished readily from normal esophageal squamous epithelium, which is pale and glossy.
There is disagreement among experts regarding the histologic type of epithelium required to confirm that there is evidence of metaplasia in the esophagus.
Virtually all would agree that the finding of an intestinal type epithelium with goblet cells (which has been called intestinal metaplasia, specialized intestinal metaplasia or specialized columnar epithelium) is clear evidence of metaplasia.

Patients who are found to have Barrett’s esophagus may be submitted to regular screening endoscopy with multiple biopsies every year or two in the hope of finding dysplasia or in situ cancer rather than allowing invasive cancer to develop and cause symptoms. There is as yet no general agreement about the benefits of screening endoscopy, nor about the ideal frequency of endoscopy. 
When Barrett’s esophagus is discovered the treatment is that of the underlying GERD. Several methods of ablation of Barrett’s mucosa are under active study, including laser, photodynamic therapy and argon beam plasma coagulation. In conjunction with high-dose PPI treatment or an antireflux operation these endoscopic methods can restore the squamous lining of the esophagus. It is not yet known whether this reduces the risk of malignant transformation since there are often remnants of glandular mucosa underneath the new squamous lining.


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