Mild intestinal metaplasia

Endoscopic mild intestinal metaplasia is a professional term. In plain words, it means that field-like epithelial cells appear in certain parts of our stomach, which makes our stomach tend to transform into the intestine. It is a pathological disease of the gastric mucosa and a chronic disease. Similar to the need for intestinal cells to slowly reproduce and differentiate, the final result is that the gastric mucosa is slowly destroyed, and diseases such as gastritis, gastric ulcer, and gastric cancer may occur in the stomach.

Intestinal metaplasia refers to the replacement of gastric mucosal epithelial cells by intestinal epithelial cells, that is, the appearance of epithelial cells similar to the mucosa of the small intestine or large intestine 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 the undifferentiated cells in the neck of the gastric glands. 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. Recently, further research has shown that the histological origin of intestinal metaplasia is mainly in the gastric groove. Tiny intestinal metaplasia foci are centered on the gastric groove and can develop into small and large intestinal metaplasia foci in the surrounding gastric areas to varying degrees. Through pathological research, a series of classifications have been made for intestinal metaplasia. According to the function of the metaplastic epithelium, intestinal metaplasia can be divided into complete or incomplete intestinal metaplasia. The former is similar to the absorptive cells of the small intestinal mucosa, with a brush border, no mucus secretion, Paneth cells, goblet cells and absorptive cells, containing sucrase, trehalase, leucine peptidase and alkaline phosphatase; while the incomplete intestinal metaplasia has an unclear brush border, underdeveloped microvilli, mucus secretion granules in the cytoplasm, containing sucrase, but low activity of aminopeptidase and alkaline phosphatase, and no trehalase.

Mucus histochemical staining can be used to divide intestinal metaplasia into small intestinal metaplasia (i.e. complete intestinal metaplasia) and colonic metaplasia (i.e. incomplete intestinal metaplasia). Colonic metaplasia has poor epithelial differentiation and a very low detection rate in benign gastric diseases (11.3%), but a high detection rate in the mucosa adjacent to intestinal type gastric cancer (88.2%), indicating that colonic metaplasia is closely related to the occurrence of gastric cancer. Generally, colonic metaplasia occurs later than intestinal metaplasia and is located in the more severe small intestinal metaplasia foci. The two types of metaplasia can coexist, so colonic metaplasia may occur on the basis of gradually worsening small intestinal metaplasia.

Chronic atrophic gastritis is often accompanied by intestinal metaplasia, which is an indicator of gastric mucosal damage and an important epithelial change in chronic atrophic gastritis. According to statistics, the rate of intestinal metaplasia combined with atrophic gastritis is 65.5%, and the rate increases with age. As the atrophic area expands, the rate of intestinal metaplasia also increases. The distribution of intestinal metaplasia and atrophic gastritis is basically the same, with the highest incidence in the gastric antrum, followed by the antral body transition area. Since atrophic gastritis and intestinal metaplasia are closely related to the occurrence of gastric cancer, such patients should be taken seriously in clinical practice, with long-term follow-up and regular examinations to prevent cancer.