A, the legacy of acute gastritis after acute gastritis, gastric mucosal lesions persistent or recurrent, can form chronic gastritis. Second, irritating foods and drugs Long-term use of diet and drugs that strongly stimulate the gastric mucosa, such as strong tea, strong alcohol, spicy or salicylate drugs, or inadequate chewing when eating, rough food repeatedly damage the gastric mucosa, or excessive smoking, tobacco oxalic acid directly on the gastric mucosa caused. Gansu Provincial Hospital of Traditional Chinese Medicine, Department of Oncology, Department of Hematology Zhanrui Third, the reflux of duodenal fluid Studies have found that patients with chronic gastritis often suffer from bile reflux due to dysfunction of the pyloric sphincter, which may be an important causative factor. Phospholipids in pancreatic juice together with bile and pancreatic digestive enzymes can dissolve mucus and destroy the gastric mucosal barrier, prompting H+ and pepsin to counter-diffuse into the mucosa and further cause damage. The resulting chronic gastritis is mainly in the gastric sinus. Gastritis due to bile reflux is common in patients undergoing gastric-jejunostomy. Peptic ulcer patients almost always have chronic sinusitis, which may be related to dysfunction of the pyloric sphincter. The nicotine in tobacco relaxes the pyloric sphincter, so long-term smokers can contribute to bile reflux and cause gastric sinusitis. The change of immune function in the pathogenesis of chronic gastritis has been widely appreciated. About 80% to 90% of patients with gastric atrophy with pernicious anemia can find antibodies to internal factors in the blood; atrophic gastritis, especially gastric gastritis patients, blood, gastric juice or in the atrophic mucosa, can often find antibodies to wall cells. Therefore, autoimmune reactions are currently considered to be the relevant etiology for some chronic gastritis. However, it is inconclusive whether immune factors are involved in the pathogenesis of gastritis. In addition, diffuse lymphocytic infiltration of the gastric mucosa in atrophic gastritis and abnormal in vitro lymphoblastoid transformation test and leukocyte movement inhibition test suggest that the cellular immune response may be important in the development of atrophic gastritis. Certain autoimmune diseases such as chronic thyroiditis, hypothyroidism or hyperthyroidism, insulin-dependent diabetes mellitus, and chronic hyperalgesia can be associated with chronic gastritis and may be related to the immune response. V. Helicobacter pylori (Hp) infection In 1982 Marshall and Warren first isolated a microaerophilic, catalase-positive, urease active gram-negative spiral bacteria, 3 μm × 0.5 μm size, curved or S-shaped end with 2 to 6 sheathed flagella. This bacterial infection is present in 95% of active gastritis, initially named Campylobacter-like organisms (CLO), later renamed Campylobacter pylori, and again renamed H. pylori in 1989 based on its biochemical and morphological characteristics (Figure 1). We confirmed through clinical studies that the detection rate of Hp in chronic active gastritis was 98% to 100%, indicating a close relationship between chronic gastritis, especially chronic active gastritis, and Hp infection. 1985 Marshall, 1987 Morris duo themselves as volunteers with oral Hp caused acute gastritis, which was cured by antibiotic treatment. 1987 Lam bert used In 1987, Lam bert used suckling pigs to successfully establish an animal model of Hp gastritis. By now, Hp has basically met the criteria for pathogenic bacteria proposed by Koch. It is now clear that Hp infection is the most important cause of chronic gastritis, which has been referred to as Hp-associated gastritis. However, other harmful physical, chemical and biological factors can also cause the disease by acting repeatedly on susceptible humans over a long period of time. Chronic lesions can develop when the cause persists or recurs. Gastric mucosal examination by random sampling in rural Finland confirmed that chronic atrophic gastritis is a chronic progressive lesion starting with superficial inflammation and ending with irreversible atrophic inflammation. There is also evidence of this from clinical observations. Young people tend to have superficial gastritis and older people tend to have atrophic gastritis; superficial gastritis and atrophic gastritis often coexist in the same patient; in addition, retrospective gastric mucosal biopsies have also found that a portion of superficial gastritis can become atrophic gastritis after several years. It is currently believed that chronic gastritis is caused by the action of multiple factors. Other chronic foci of infection in the nasal cavity, oral cavity, and pharynx that involve the gastric mucosa can cause chronic gastritis. Heart failure or portal hypertension can leave the stomach in a state of long-term stasis, resulting in continuous hypoxia and nutritional disorders of the gastric mucosa, which can lead to gastric mucosal degeneration and cause chronic inflammation of the gastric mucosa. The lack of gastric acid makes it easy for bacteria to multiply, which can also cause gastritis. Some people also summarize the 10 causes of chronic gastritis: (1) bacteria, viruses or their toxins: mostly seen after acute gastritis, gastric mucosal lesions that do not heal over time and develop into chronic superficial gastritis. (2) irritants: long-term drinking of strong alcohol, strong tea, strong coffee and other irritants can destroy the protective barrier of the gastric mucosa and gastritis occurs. (3) Drugs: Some drugs such as salicylates, digitalis, pau d’arco, anti-inflammatory pain, cinchofen, etc. can cause chronic gastric mucosal damage. (4) Chronic infection of the oral cavity and pharynx. (5) Bile reflux; bile salts contained in bile can destroy the gastric mucosal barrier and cause inflammation by counter-diffusion of hydrogen ions from gastric juice into the gastric mucosa. (6) X-ray irradiation: deep X-ray irradiation of the stomach can cause damage to the gastric mucosa and produce gastritis. (7) Helicobacter pylori infection. (8) Earth physical changes: such as environmental changes, climate change, if people can not adapt in a short period of time, it can cause the nerve dysfunction of the stomach, gastric secretion and gastric movement is not coordinated, resulting in gastritis. (9) Long-term mental tension, irregular life. (10) The impact of other organ lesions: such as chronic, uremia, ulcerative nodes, chronic, etc. can cause chronic gastritis.