Barrett's Esophagus (cont.)
In this Article
- Barrett's esophagus facts
- What is Barrett's esophagus?
- Why is there so much interest in Barrett's esophagus?
- What causes Barrett's esophagus?
- Who develops Barrett's esophagus?
- What is the specific abnormality in the inner lining (epithelium) of Barrett's esophagus?
- What about the cancer that occurs in Barrett's esophagus?
- What is dysplasia in Barrett's esophagus?
- What is the risk of developing adenocarcinoma of the esophagus in Barrett's?
- What are the symptoms of Barrett's esophagus?
- How is GERD with or without Barrett's esophagus treated?
- Why is it important to screen patients with GERD to diagnose Barrett's esophagus?
- Why is it critical to be accurate in the diagnosis of Barrett's esophagus?
- What does endoscopic biopsy surveillance in Barrett's esophagus involve?
- How is high grade dysplasia managed?
- How is low grade dysplasia managed?
- What are the experimental approaches for treatment of high grade dysplasia?
- What experimental options are there for Barrett's esophagus WITHOUT dysplasia?
- What does the future hold for Barrett's esophagus?
- Find a local Gastroenterologist in your town
Who develops Barrett's esophagus?
A significant percentage of individuals with chronic symptoms of GERD develop Barrett's esophagus, and it is most common in Caucasian male populations. Not everyone with GERD has symptoms of GERD, however. Therefore, some people with Barrett's are unaware that they have Barrett's because they have GERD without any symptoms at all or have very mild and infrequent symptoms.
It is unclear why Barrett's esophagus is so overwhelmingly more common in white males than in any other group. For example, although women and African-Americans do not seem to be protected from developing GERD, they are largely protected (especially African-Americans) from developing Barrett's esophagus and Barrett's cancer (adenocarcinoma). There is evidence that in the western hemisphere, esophageal cancer and cancer of the gastroesophageal junction (called cardia cancer) are increasing in frequency, perhaps more so than any other gastrointestinal tract cancer. (However, colon cancer is still very much more common than esophageal cancer.)
Barrett's esophagus may run in some families and be genetically determined. Studies are underway to determine if any genes or markers can be found in these families that would predict the development of Barrett's esophagus in the general population. In these families with Barrett's as well as with Barrett's in the general population, GERD is the common denominator. However, the question is why the Barrett's occurs more commonly in these families than in others with comparably severe GERD, but with no family association.
What is the specific abnormality in the inner lining (epithelium) of Barrett's esophagus?
To repeat, the first criterion for the diagnosis of Barrett's esophagus is the finding at endoscopy of a pink lining in the esophagus where it is normally not seen. This abnormal lining may appear circumferentially like a band, tongue-like or as islands. The second criterion is that biopsies from the pink lining reveal the characteristic intestinalized mucosa (the lining normally seen in the intestines) with the typical goblet cells. The esophageal biopsies are obtained during an endoscopy. An upper gastrointestinal endoscopy is a procedure in which the doctor inserts a long flexible tube (endoscope) through the mouth and down into the esophagus to directly visualize the lining of the esophagus. During the same endoscopic examination, the stomach and duodenum also can be visualized. Multiple small samples (biopsies) of the lining epithelial tissue can be obtained through the endoscope.
As mentioned previously, the process of the replacement of one type of tissue lining by another is called metaplasia. In the stomach and intestines, metaplasia is a common response to certain types of injury. As Henry Appelman, a pathologist, stated: "When the gut is under stress it wants to be something else." Other examples of metaplasia in which one lining replaces another are: (1) in the stomach where chronic inflammation (gastritis) may result in an intestinal-type lining replacing parts of the normal stomach lining; and (2) in the duodenum (just beyond the stomach in the intestine) where peptic ulcers occur and the intestinal lining surrounding the ulcer transforms into stomach-type lining.
We believe that the process of metaplasia is a protective or adaptive response to injury of the lining. However, the downside of metaplasia is that in Barrett's esophagus, it carries a small but definite increase in the risk of becoming cancerous. Not all metaplasias have an increased risk of cancer. For example, of the two metaplasias referred to in the previous paragraph, intestinal metaplasia in the stomach can lead to cancer, but intestinal metaplasia in the duodenum does not.
The process of developing Barrett's begins at the junction of the stomach and esophageal linings. The esophagus normally is lined by a squamous epithelium or lining layer. This squamous epithelium has a pearly white appearance, whereas the lining in the stomach and intestines has a more salmon pink color because it is a columnar epithelium rather than a squamous epithelium. The squamous epithelium is made up of flat squamous cells, which are similar to skin cells. The stomach or gastric lining consists of taller columnar cells as seen under the microscope. The junction of the squamous epithelium of the esophagus and the gastric columnar epithelium occurs at the junction of the esophagus and stomach where, as you recall, the lower esophageal sphincter is located. The common border (interface) of these two linings is often referred to as the Z line, because when examined during an endoscopy, it has a zig zag appearance.
With progressive injury to the esophagus, metaplasia occurs and the metaplastic tissue moves up the esophagus for a distance which varies from person to person, usually from about 0.5 to 2.5 inches (about 1 to 6 centimeters). The type of cell that gives rise to the metaplastic tissue is not known.
Barrett's esophagus often is categorized into short- or long-segment Barrett's, based on the length of the esophagus that is affected. Short segment Barrett's generally refers to involvement of 3 centimeters or less while long segment means involvement of more than 3 centimeters of the esophagus. Interestingly, once Barrett's esophagus is diagnosed in a patient, the metaplastic lining does not seem to progress further up into the esophagus if the patient is being treated for GERD. Thus, over time, the length of involvement with Barrett's generally remains the same.
Intestinal metaplasia of the Z line (gastroesophageal junction) without visible Barrett's
If biopsies are taken from patients with GERD who have a normal appearing Z line (no visible evidence of Barrett's esophagus), up to 30% will show the same intestinal type metaplasia with goblet cells as those that are seen in Barrett's esophagus. However, we do not routinely biopsy normal appearing Z lines to look for this change, nor do we do surveillance when we find it there. The reason is that limited intestinal metaplasia of the gastroesophageal junction region in GERD seems to occur with similar frequency in women and African Americans as in white men, yet the risk of overt Barrett's esophagus is much less than in white men.
Therefore, the presence of metaplasia on a routine biopsy of a normal appearing Z line in GERD should not lead to any change in management. What's more, the finding of goblet cells in this context should not be labeled, as some have suggested, as ultrashort segment Barrett's. The main reason for not labeling it as Barrett's is that the term Barrett's implies an increased risk of cancer, and there is no evidence that this finding is associated with an increased cancer risk.
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