Pseudopyloric metaplasia is seen only in atrophic gastritis. The metaplasia is divided into intestinal glandular metaplasia and pseudopyloric metaplasia, which refers to the replacement of the gastric body mucosa by the mucosa of the gastric sinus, often migrating upward along the gastric lesser curvature, called sinus subterranean migration. Atrophic gastritis is a pathological change in which the intrinsic mucosal glands atrophy or even disappear after repeated damage to the gastric mucosal surface, and thickening of the mucosal muscle layer is common. Due to the atrophy or disappearance of the glands, there is varying degrees of thinning of the gastric mucosa, often accompanied by intestinal epithelial metaplasia, inflammatory reaction and atypical hyperplasia. The disease is one of the common diseases of the digestive system, and the incidence of chronic gastritis is very high in our general population, with atrophic gastritis accounting for 13.8% of those examined. Chronic atrophic gastritis is mostly caused by the failure or mismanagement of chronic superficial gastritis, and a few atrophic gastritis can evolve into gastric cancer. What are the causes of pseudopyloric hyperplasia? It may be related to the following factors: 1. Biological factors: The impact of chronic infectious diseases such as hepatitis and tuberculosis on the stomach has also attracted attention. Patients with chronic liver disease often have signs and symptoms of chronic gastritis, and gastric mucosal staining has also confirmed the presence of antigenic antibody complexes of hepatitis B virus in the gastric mucosa of hepatitis B patients. Ruijin Hospital reported 91 cases of atrophic gastritis, 24 cases (26.4%) were combined with chronic hepatitis. So chronic infectious diseases, especially chronic liver disease on the stomach is worth noting. 2, physical factors: clinical statistics show that the occurrence of this disease is significantly positively correlated with age. The older the person is, the poorer the “resistance” of the gastric mucosa function, and the more susceptible to damage caused by adverse external factors. 3, bile or duodenal fluid reflux: due to pyloric sphincter dysfunction or after gastrojejunostomy, bile or duodenal fluid can reflux into the stomach and destroy the gastric mucosal barrier, prompting H?+ and pepsin to backscatter into the mucosa causing a series of pathological changes, resulting in chronic superficial gastritis, and can develop into chronic atrophic gastritis. 4, immune factors: in atrophic gastritis, especially gastric gastritis patients with blood, gastric juice or in the plasma cells of the atrophic mucosa, can often find wall cell antibodies or endogenous factor antibodies, it is believed that the autoimmune response is the relevant cause of chronic atrophic gastritis. In recent years, a few patients with gastric sinus gastritis were found to have antibodies to gastrin-secreting cells, which are specific autoimmune antibodies to cells and belong to the Ig G lineage. Some patients with atrophic gastritis have abnormal in vitro lymphocyte transformation test and leukocyte movement inhibition test, suggesting that cellular immune response is also important in the development of atrophic gastritis. 5, Helicobacter pylori (HP) infection: In 1983, Australian scholars Marshall and Warren first isolated HP from the mucus layer and epithelial cells of the gastric sinus in patients with chronic gastritis. since then many scholars have conducted numerous experimental studies on patients with chronic gastritis, and HP was cultured in the gastric mucosa of 60% to 90% of patients with chronic gastritis, and then found that the degree of HP infection was associated with At the 8th meeting of the World Gastroenterology Association in 1986, it was suggested that HP infection is one of the important causes of chronic gastritis. In addition, such as improper diet, long-term addiction to tobacco and alcohol, drug abuse, chronic inflammation of the upper respiratory tract, central nervous system dysfunction, damage to the gastric mucosa, as well as the removal of the gastric sinusoidal area that secretes gastrin after major gastrectomy, resulting in the atrophy and inflammatory changes of the gastric mucosa, are all prone to damage to the gastric mucosa.