The occurrence of CAG is the result of a combination of factors, related to Hp infection, immunity, duodenal fluid reflux, genetics, age, high salt and low vitamin diet, etc. Hp infection is the main cause of chronic gastritis (80%-95%), and is also one of the important causes of CAG, after long-term infection (about 5-25 years), some patients can have gastric mucosal atrophy and intestinalization. (1) Hp causes cellular damage through ammonia production and secretion of vacuolar toxin A (vacA); (2) cytotoxin-associated gene A (cagA) protein can cause strong inflammatory reaction in gastric mucosa; (3) bacteriophage cell wall can (3) the cell wall of the bacterium can act as an antigen to induce immune reflection. The long-term presence of these factors leads to chronic inflammation of the gastric mucosa, the latter of which can lead to destruction of the intrinsic gastric glands and atrophy. 2, Other infections Infection of other pathogenic microorganisms in the gastric mucosa is also correlated with the occurrence of CAG. Some studies have reported an increased detection rate of EBV in patients with CAG, and EBv infection may play an important role in the progression of CAG to gastric cancer. In some areas, the detection rate of fungi in gastric juice of CAG patients is high. Immune mechanisms: 1. Autoimmune gastritis Chronic gastritis with a predominantly atrophic gastric body occurs on an autoimmune basis, or type A gastritis. The patient has autoantibodies in the blood, namely intrinsic factor antibody (IFA) and parietal cell antibody (PCA). IFA is divided into two types: type I, also known as blocking antibody, prevents vitamin B12 from binding to intrinsic factor, so that vitamin B12 cannot be absorbed; type II, also known as binding antibody, binds to the intrinsic factor vitamin B12 complex, preventing the absorption of vitamin B12 and leading to pernicious anemia. Mural cell antibodies (PCA) in general atrophic gastritis positive rate of 20% ~ 60%, can reduce the total number of mural cells, leading to a decrease in gastric acid secretion or lack of. 2, other immune factors Nandelli used the gastric mucosa of type B atrophic gastritis to act on various autoimmune antibodies and found gastrin secretory cell antibody (GCA).GCA is related to type B atrophic gastritis. GCA is a specific autoimmune antibody to G-cell plasma, which belongs to the IgG family and has complement binding ability, suggesting that in some patients with type B, the lesion is related to G-cell autoimmunity. However, only 10% of gastric sinusitis has GCA, so other causative factors need to be studied. Cellular immunity: such as lymphocyte transformation, macrophage mobile inhibition, various skin tests and tumor cell killing tests confirm the presence of cellular immunity in chronic gastritis. lymphocytes are commonly seen in the gastric epithelium of CAG, and in some cases mitosis or pseudopods of lymphocytes have been observed, leading to the phenomenon of plasma membrane lysis of adjacent wall cells, indicating that the phenomenon of cellular immunity occurs simultaneously with gastric mucosal lesions during the pathogenesis. Third, duodenal fluid reflux Duodenal fluid reflux, a large amount of bile, pancreatic and intestinal fluid reflux into the stomach, weakening the gastric mucosal barrier function, so that the gastric mucosa is subjected to the action of digestive juices, resulting in inflammation, erosion, bleeding and mucosal epithelial atrophy, chemogenic changes, etc.. Bile reflux is considered to be one of the causative factors of CAG. Bile reflux can damage the gastric mucosal barrier, and H+ in the gastric lumen is back-diffused into the gastric mucosa through the damaged barrier, stimulating increased secretion of histamine, which acts on vascular H1 receptors and H2 receptors causing vasodilation, increased permeability, decreased effective blood flow to the gastric mucosa, and weakened mucosal repair; at the same time, histamine can increase gastric acid secretion and aggravate gastric mucosal damage, thus leading to the occurrence of CAG. In addition, reflux can stimulate gastrin release to inhibit the pyloric sphincter, causing bile reflux to form a vicious circle. Some reports show that the proportion of atrophy, intestinal metaplasia and heterogeneous hyperplasia of gastric mucosa in patients with bile reflux gastritis is significantly higher than that in the non-bile reflux group, and the difference is significant (P<0.05). IV. Other factors 1 Age The incidence of CAG increases with age, and atrophy, intestinalization, and heterogeneous hyperplasia also increase and worsen with age. This may be due to small arteriosclerosis and degenerative changes in the gastric mucosa in the elderly, resulting in malnutrition of the mucosa, decreased secretory function and reduced gastric mucosal barrier function, which become important factors in the occurrence of CAG in the elderly. 2 , nutritional factors vitamin deficiency: the high incidence of CAG in the age of 50 years or older, a large number of clinical data have clearly suggested that the elderly population vitamin B12, folic acid deficiency. Long-term Hp infection will inhibit the secretion of vitamin C from the gastric mucosa, so that the scavenging ability of vitamin C for oxygen free radicals and nitrite is reduced, thus aggravating the degree of CAG lesions. Gastric mucosal trophic factor deficiency: such as gastrin, epidermal growth factor, gastrin suppression, etc., or insensitivity of gastric mucosal sensory nerve terminals to these factors can also cause gastric mucosal atrophy. Chronic iron deficiency and ischemia and hypoxia can cause damage to the gastric mucosa. Certain trace elements such as zinc and selenium deficiency can affect the oxygen radical scavenging enzyme activity, for gastric mucosa damage may be related. 3, physical and chemical factors Lifestyle: At present, domestic and foreign scholars generally believe that the occurrence of CAG and lifestyle, dietary habits have a great relationship, long-term repeated consumption of strong irritating foods such as strong alcohol, strong tea, coffee, kimchi, too hot or too cold diet, too little intake of fruits and vegetables are related to the occurrence of CAG. Medications: Non-steroidal anti-inflammatory drugs (NSAIDs) such as aspirin and Protaxon can cause gastric mucosal erosion, and chronic gastritis can remain after the erosion heals. Some antibiotics also have some damage to the gastric mucosa, but there is no evidence that long-term use can cause CAG. Metal exposure and radiation: Heavy metals such as mercury, copper and zinc have some damaging effect on the gastric mucosa, such as lead workers gastric mucosal biopsy found an increased incidence of CAG, Palmer called excretory gastritis (excretion gastritis). Radiation therapy for ulcer disease or other tumors can cause damage to the gastric mucosa or even atrophy. 4, genetic According to Varis survey, the incidence of CAG patients is significantly higher among the first generation of relatives, and the genetic predisposition to pernicious anemia is also obvious, compared with the control group is 20 times larger, the human hereditary predisposition to susceptibility is an important physical condition for the development of this part of CAG.