written by: Eric Haines
• edited by: Emma Lloyd
• updated: 7/1/2010
Focal intestinal metaplasia is the potentially reversible change from a fully differentiated stomach cell type to an intestinal cell type. It is associated with significantly increased risk of cancer. . Proper diagnosis and treatment can reduce the risk of gastric cancer
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Metaplasia is the potentially reversible change from a fully differentiated cell type to another cell type. Metaplasia is associated with significantly increased risk of cancer. Therefore, it is defined as a precancerous condition. Metaplasia can occur in a variety of the body’s tissues. However, it is most commonly found in the stomach or intestines. The condition in which stomach cells become similar to intestinal cells is called focal intestinal metaphasia
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Causes and Symptoms
Focal intestinal metaplasia is associated with H pylori infection, with intestinal metaplasia progression in almost half of H pylori positive patients. Moreover, it has been shown that eradication of H pylori can reverse intestinal metaphasia and thus reduce the risk of gastric cancer. While targeting H pylori has been successful in reversing intestinal metaphasia, it is important to note that other genetic and environmental factors can influence metaphasia and the development of gastric cancer.
These other factors include:
Lack of vitamin C
Bacterial and nitrate-related DNA damage
Previous surgical history
COX-2 expression (An enzyme that causes inflammation and pain and fever and that is generally targeted by NSAIDs)
Another mechanism responsible for intestinal metaphasia is bile reflux. The reflux of bile into the stomach can damage the gastric mucosa and make the stomach susceptible to metaphasia.
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Intestinal metaphasia is a symptom of Gastritis
Gastritis is the inflammation of the gastric mucosa. It is caused by several factors such as, H pylori infection, NSAIDs, alcohol, stress and autoimmune diseases. Chronic gastritis is associated with atrophy (loss of function of the mucosa) or metaplasia. There are two types of metaplasia commonly found in chronic gastritis:
Mucous gland metaplasia
It is characterized by the replacement of gastric glands with mucous glands. Gastric ulcers tend to be present in this condition. However, it still not fully elucidated whether these ulcers are the cause or consequence of the metaplasia.
Focal intestinal metaplasia
It is typically in response to chronic mucosal injury. The gastric mucosa cells change to resemble those of the intestinal mucosa. Intestinal metaplasia can be classified as either complete, a condition in which all the gastric mucosa have been transformed into small-bowel mucosa, or incomplete, where the epithelium assumes an appearance similar to that of the large intestine.
Intestinal metaplasia is also a common in Barrett esophagus. It this condition it is the esophageal squamous epithelial cells that undergo metaplasia. Approximately, 60% of esophageal cancers diagnosed in the U.S. stem from focal intestinal metaplasia.
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Practitioners must first learn to differentiate focal intestinal metaphasia of the stomach from dysplasia. The difference between the two is; intestinal metaphasia is a precancerous condition and dysplasia is a precancerous lesion. In other words, intestinal metaphasia is a condition that increases the risk of developing gastric cancer, whereas dysplasia is an abnormality or symptom that present in some cancerous conditions. The differential diagnosis of these two similar conditions is important in treatment selection.
Biopsy is the most common mean of diagnosis focal intestinal metaphasia. However, a diagnosis of intestinal metaphasia is missed in approximately half of all biopsies. To improve diagnostic numbers, it is recommended that the biopsy be taken in areas of whitish plaques, patches or homogeneous discoloration.
Both the Extent and location of intestinal metaplasia factor into the identification of patients at a higher risk of cancer.
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While the efficiency of H pylori eradication in treating focal intestinal metaphasia is still controversial, there are reports of intestinal metaphasal regression following eradication treatments. Other studies suggest that the effectiveness of H pylori eradication requires the assistance of anti-oxidant agents. Moreover, an Italian study has demonstrated that co-administration of ascorbic acid, a sugar acid with anti-oxidant properties, with H pylori eradication significantly resolved intestinal metaphasia of the stomach. Even more importantly, a Colombian study showed that anti-H pylori treatment and anti-oxidant dietary supplementation may play an anti-cancerous roleand reduce patient’s risk of developing gastric cancer.