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Intestinal metaplasia is the transformation of epithelium (usually of the stomach or the esophagus) into a type of epithelium resembling that found in the intestine. In the esophagus, this is called Barrett's esophagus .
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.
Adenocarcinomas of the esophagus tend to arise in a field defect called Barrett's esophagus, a red patch of tissue in the generally pink lower esophagus. A diagnosis of Barrett's esophagus is confirmed by a metaplastic change of the esophageal mucosa from squamous to columnar mucosa with intestinal metaplasia.
Micrograph showing apocrine metaplasia of the breast with typical features [3] H&E stain. Barrett's esophagus is an abnormal change in the cells of the lower esophagus, thought to be caused by damage from chronic stomach acid exposure. The following table lists some common tissues susceptible to metaplasia, and the stimuli that can cause the ...
Esophageal strictures – the persistent narrowing of the esophagus caused by reflux-induced inflammation; Barrett's esophagus – intestinal metaplasia (changes of the epithelial cells from squamous to intestinal columnar epithelium) of the distal esophagus [20] Esophageal adenocarcinoma – a form of cancer [17]
Esophageal diseases can derive from congenital conditions, or they can be acquired later in life. Many people experience a burning sensation in their chest occasionally, caused by stomach acids refluxing into the esophagus , normally called heartburn.
Recent research has shown that autoimmune metaplastic atrophic gastritis (AMAG) is a result of the immune system attacking the parietal cells. [6]Environmental metaplastic atrophic gastritis (EMAG) is due to environmental factors, such as diet and H. pylori infection.
Owing to the causal relationship between H. pylori infection and gastric MALT lymphoma, identification of the infection is imperative. Histological examination of GI biopsies yields a sensitivity of 95% with five biopsies, [7] but these should be from sites uninvolved by lymphoma and the identification of the organism may be compromised by areas of extensive intestinal metaplasia.