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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 .
Intestinal metaplasia typically begins in response to chronic mucosal injury in the antrum and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is ...
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.
This includes patients diagnosed with gastric adenocarcinoma (especially those with early-stage disease), patients found to have atrophic gastritis or intestinal metaplasia, as well as first-degree relatives of patients with gastric adenocarcinoma since the relatives themselves are at increased risk of gastric cancer partly due to the ...
The presence of intestinal metaplasia in Barrett's esophagus represents a marker for the progression of metaplasia towards dysplasia and eventually adenocarcinoma. This factor combined with two different immunohistochemical expression of p53, Her2 and p16 leads to two different genetic pathways that likely progress to dysplasia in Barrett's ...
Intestinal metaplasia is a premalignant condition that increases the risk for subsequent gastric cancer. [4] Intestinal metaplasia lesions with an active DNA damage response will likely undergo extended latency in the premalignant state until further damaging hits override the DNA damage response leading to clonal expansion and progression. [4]