Strick land classified atrophic gastritis into two types, A and B, based on the site of occurrence of atrophic gastritis combined with immunological changes, including autoimmune tests and serum gastrin assays. Type A atrophic gastritis is an autoimmune disease with positive autoantibodies. Since the autoimmune damage occurs in the mural cells, the lesions are heavier in the gastric body, and the gastric body glands are destroyed and atrophied, so gastric acid secretion is significantly reduced or absent, and as a result, serum gastrin levels are increased, which can eventually develop into gastric atrophy. Type A patients are often associated with pernicious anemia (16%), and 60% of these pernicious anemias have blocked IFA. atrophic gastritis in China is mainly seen in the gastric sinus and occurs less in the gastric body, which is consistent with the fact that there is very little pernicious anemia in China. Type B atrophic gastritis is not an immune disease and is autoantibody negative. Its pathogenesis is related to duodenal fluid reflux or other chemical or physical damage, and the mucosa of the gastric sinus is more permeable than that of the gastric body (the ability of H+ to reverse diffuse is 20 times stronger in the gastric sinus than in the gastric fundus). Since the mucosal barrier of the gastric sinus is smaller than that of other parts of the stomach, it is vulnerable to the reflux of duodenal fluid and its contents, so the gastric sinus is the most vulnerable. Gastric body lesions are mild, so gastric acid secretion is generally normal. G-cells in the pyloric gland are damaged by the sinus lesions, and gastrin secretion is reduced, so serum gastrin levels are generally low. The carcinogenesis of atrophic gastritis is predominantly type B, and the carcinogenesis process can last for more than 10 years or longer.