We often encounter this situation in our normal clinical work, doctor, my pathology report came out, there is intestinal epithelial hyperplasia, do you think it is cancerous, will it be cancerous? First of all, we should clarify what is intestinal epithelial hyperplasia. Intestinal epithelial metaplasia (referred to as intestinal chemistry) is a relatively common phenomenon, especially in senior people. Intestinal epithelial hyperplasia is often combined with chronic gastritis, especially chronic atrophic gastritis. It is the pathological transformation of the gastric mucosal epithelium and its glands into intestinal mucosal epithelium and glands. It is mainly divided into 4 types: (1) Complete small intestine type: histomorphology resembles small intestine mucosal epithelium, visible absorptive cells with obvious striated edges, cup cells and a few Pan cells, cup cells contain sialic acid mucus but not sulfate mucus, absorptive cells do not contain mucus. (2) Incomplete small intestine type: In addition to cup cells and absorptive cells, some absorptive cells were replaced by columnar mucus cells, and no Pan’s cells were present. The cup-shaped cells contain sialic acid mucus but not sulfate mucus, and the columnar cells contain only neutral mucus. (3) Complete colorectal type: Absorbent cells with obvious striated rim, cup cells and Pan’s cells were seen. The cup-shaped cells contain sulfate mucus, and the absorptive cells do not contain mucus. (4) Incomplete colorectal type: Absorbent cells are partially or completely replaced by columnar mucous cells, no Pan’s cells are present, and cup cells contain sulfate mucus. Of course, this is a strict medical classification, only the physician engaged in pathology can divide it very clearly, our pathological results are not so detailed, know the general classification on the line. Incomplete colon type intestinal chemosis mainly exists in the paracancerous tissues, accounting for 78.71%, so it is closely related to the occurrence of intestinal type gastric cancer. Incomplete small intestine intestinal metaplasia mainly exists in the background mucosal tissue and is widely seen in various benign gastric diseases, especially in chronic gastritis, which is a reversible lesion. However, incomplete small intestinal metaplasia can also worsen with the progression of inflammation and transform to incomplete large intestinal metaplasia. Gastric mucosal intestinal epithelial metaplasia is quite common and increases with age, with a detection rate of 30% in the 20-30 age group and up to 80% in the 50-60 age group. The exact cause is unclear, and its appearance may be related to gastric mucosal damage and incomplete regenerative repair. Recent studies have found that there is also a relationship between H. pylori infection and intestinal epithelial metaplasia. Intestinal epithelial metaplasia is not necessarily carcinogenic. Generally speaking, small intestine type chemosis or complete intestinal epithelial chemosis with good epithelial differentiation is seen in various benign gastric diseases, especially in chronic gastritis, and the chemosis worsens with the development of inflammation, so it is thought that this type of chemosis may belong to the nature of inflammatory response and has little relationship with gastric cancer. In contrast, colorectal type chemosis or incomplete intestinal epithelial chemosis with poor epithelial differentiation has a lower detection rate in benign gastric disease, but a higher detection rate in the mucosa adjacent to intestinal gastric cancer, indicating that this type of chemosis is related to the occurrence of gastric cancer. Chronic infection of HP plays an important role in intestinal chemosis and is considered a class I carcinogenic factor. Its pathogenesis may be: (1) HP can cause damage to mucosal inflammation and increase the chance of DNA damage; (2) inflammation in the HP-infected area, there is cellular peroxidation damage, and damage to the gastric mucosal barrier induces carcinogenesis; (3) HP itself can also produce a variety of enzymes and toxins that cause DNA damage, oncogene inactivation (4) HP infection can cause a decrease in gastric acid secretion, which is conducive to the growth of other bacteria in the stomach and the increase of nitrite substances that cause cancer. Therefore, HP eradication refers to the early detection and early diagnosis of enterochemical with important guiding value. However, studies have found that HP eradication is only beneficial for patients with atrophic gastritis and not intestinal chemosis, which indicates that prophylactic HP eradication should be performed before chemosis occurs. What should I do if intestinal metaplasia occurs? The occurrence of gastric cancer generally goes through the process of: normal gastric mucosa → chronic superficial gastritis → chronic atrophic gastritis → incomplete small intestinal type enterosis → incomplete large intestinal type enterosis → heterogeneous hyperplasia → early gastric cancer → progressive gastric cancer. In addition to the necessary medication and regular review, the most important thing is to pay attention to the regulation of diet, avoiding the stimulation of gastric mucosa by stimulating foods such as tobacco, alcohol, too acidic and spicy, cold and greasy, so as to slow down the progress of intestinalization. Chinese medicine treatment of intestinal chemistry and chronic atrophic gastritis is the same, generally a year of treatment for three months, mainly to identify the evidence of treatment, mainly tonics, supplemented by external treatment, the effect is good, may make some patients with intestinal chemistry back to normal.