What does gastric glandular intestinal metaplasia mean?

To put it simply, gastric glandular intestinal metaplasia means that the gastric glands have a tendency to resemble intestinal lesions. To put it more professionally, the cells of the gastric surface mucosal epithelium are gradually replaced by new intestinal cells. It is a common gastric mucosal lesion and a precursor to many chronic diseases. The various organs in our body have their own functions. As the surface of our stomach is gradually occupied, it is conceivable that the stomach function will be affected, and in the later stages it may develop into stomach cancer.

It refers to the replacement of gastric mucosal epithelial cells by intestinal epithelial cells, that is, the appearance of epithelial cells similar to the small intestine or large intestine mucosa in the gastric mucosa. It is a common lesion of the gastric mucosa and is seen in many chronic gastric diseases. Intestinal metaplastic cells originate from undifferentiated cells in the neck of the gastric glands. Some of these cells are proliferation centers and have the potential to differentiate into gastric and intestinal epithelial cells. Under normal circumstances, it continuously differentiates into gastric-type epithelial cells to replenish the aging and shed surface epithelium; under pathological conditions, it can differentiate into intestinal-type epithelial cells to form intestinal metaplasia.

Intestinal metaplasia refers to the appearance of intestinal glandular epithelium in the gastric mucosa, especially in the pyloric gland area. From the perspective of general histopathological observation, the metaplastic intestinal glandular epithelium is very similar to the small intestinal epithelium in morphology and function, but some intestinal epithelial metaplasia is very similar to the large intestinal epithelium. The intestinal epithelium includes absorptive cells, goblet cells and Paneth cells. The mucus secreted by metaplastic intestinal epithelial cells is different from the mucus secreted by the gastric mucosa. The former is mainly acidic mucin, while the latter is mainly neutral mucin.

The pathological findings of the red mucosa were mainly lymphocytes and plasma cells, with neutrophil infiltration and varying degrees of glandular atrophy and intestinal metaplasia (IM) in 7 cases, and the remaining 20 cases were chronic superficial gastritis and chronic atrophic gastritis. Intestinal metaplasia accounted for 25.9% of all erythematous mucosa. Among these 7 patients with intestinal metaplasia, 4 had a family history of gastric cancer, and the other 3 had a long history (8 to 20 years). The clinical characteristics of these 7 patients were that they all had long-term upper abdominal discomfort, acid reflux, belching, heartburn and other symptoms of varying severity. They had never used any stomach medicine. When they sought medical treatment, the clinical symptoms of 4 of them were significantly aggravated, mainly abdominal pain and heartburn, while the symptoms of the other 3 were mild. After symptomatic treatment, the clinical symptoms of the seven patients disappeared and the intestinal metaplasia components disappeared in pathological examination.