【Treatment】 (a) Diet and removal of unfavorable factors Eat a light diet, avoid irritating foods, rough foods, overheated drinks, alcohol abuse, salty foods, etc. The most important thing is to find and remove as many causes of chronic gastritis as possible, stopping medication, alcohol, smoking, etc. （The fear of chronic gastritis is more inclined to the fear that gastritis will become cancerous. Some clinical observations have found that neuroendocrine dysfunction and imbalance of gastrointestinal hormone release play a role in the pathogenesis of chronic gastritis. The lifestyle of patients with autonomic dysfunction manifested by tension, anxiety, agitation, irritability, and sadness should be given adequate attention in the treatment. At present, only atrophic gastritis is related to gastric cancer, so patients should be given proper health education to maintain an optimistic attitude towards life and avoid aggravating their mental burden. （The main function of gastric mucosal protective drugs is to enhance the barrier function of gastric mucosa and strengthen the ability of gastric mucosa to resist damaging factors. For those who have acid reflux, heartburn, stomach pain and gastroscopy suggesting mucosal erosion and bleeding, mucosal protective agents can be given. (1) Aluminum thiosulfate The aluminum salt of sucrose sulfate containing 8 sulfate roots can dissociate sucrose sulfate complex ions under acidic environment, and the complex ions polymerize into insoluble negatively charged colloids, which can combine with positively charged protein exudates at the ulcer or inflammation to form a protective film covering the surface of the lesion, preventing further invasion by damaging factors such as gastric acid and pepsin and promoting healing of the broken mucosa. Aluminum thioglycollate also has the effect of adsorbing pepsin, neutralizing gastric acid and bile acid, and promoting the synthesis of endogenous prostaglandin E as well as adsorbing epidermal growth factor to concentrate at the ulcer or inflammation, which is conducive to mucosal regeneration. Dosage and precautions: Thioglycollate 1g, 3-4 times daily, chewed 1 hour before meals and at bedtime on an empty stomach. Adverse reactions are commonly constipation, individual patients may experience dry mouth, nausea, rash, stomach cramps, etc. Continuous application should not exceed 8 weeks, and long-term high dose may cause phosphorus deficiency in body fluids, so it should not be taken for a long time by patients with hypophosphatemia such as hyperthyroidism and rickets. Complexation with pepsin in multi-enzyme tablets and pancreatic enzymes reduces their efficacy, so they should not be combined (2) Bismuth forms a diffuse protective layer in the gastric acid environment, covering the mucosal surface, isolating the erosion surface and ulcer foci from gastric acid and pepsin, playing a protective role for the damaged mucosa, promoting the repair and healing of damaged mucosal tissue; reducing pepsin activity and increasing mucin secretion; can stimulate endogenous It can stimulate the production of endogenous prostaglandins and epidermal growth factor, accelerate the healing of wounds and the disappearance of inflammation, and also has a certain hemostatic effect. It has a killing effect on Helicobacter pylori. Dosage and precautions: Bismuth potassium citrate 110mg 4 times a day, the first 3 times half an hour before 3 meals and the 4th time 2 hours after dinner; or 2 times a day, 220mg in the morning and 220mg in the evening. bismuth pectin 150-200mg 4 times a day. It may cause ammonia taste in the mouth and make the tongue and stool grayish-black, which will disappear on its own after stopping the drug; occasional nausea and constipation may be seen. Continuous use should not exceed 8 weeks. (3) Teprenone Animal tests have proved that teprenone has strong anti-ulcer effect and improvement of gastric mucosal lesions; it can promote the synthesis and secretion of mucus; it can increase the prostaglandin effect in gastric mucosa by increasing prostaglandin biosynthetic enzyme activity, which in turn increases and improves gastric mucosal blood flow; it also has the effect of maintaining the in vivo homeostasis of cells in the proliferative zone of gastric mucosa and inhibiting lipid peroxidation. Dosage and Precautions: Teprenone 50mg Tid. side effects include: constipation, diarrhea, vomiting, thirst, abdominal pain, abdominal distension. Transient elevation of transaminases. Other rare headache, rash, pruritus. 2.Gastric motivational drugs For fullness and discomfort, belching can be given gastrointestinal motivational drugs. (1) morpholine is a peripheral dopamine receptor blocker, acting directly on the gastrointestinal wall, can increase the tension of the lower esophageal sphincter, prevent gastroesophageal reflux, enhance gastric motility, promote gastric emptying, coordinate gastric and duodenal movements, inhibit nausea, vomiting, and can effectively prevent bile reflux, does not affect gastric secretion. Usage and precautions: Morpholine 10mg Tid or Qid. Since it does not easily pass the blood-cerebrospinal fluid barrier and has no inhibitory effect on dopamine receptors in the brain, there are no neurological or psychiatric adverse effects such as extrapyramidal, but it should be used with caution in children because of their imperfectly developed blood-cerebrospinal fluid barrier. Sometimes serum prolactin levels may be increased. (2) Mosapride is a selective 5-hydroxytryptamine 4 (5-HT4) receptor agonist, which promotes the release of acetylcholine through excitation of 5-HT4 receptors in the cholinergic interneurons and intermuscular plexus of the gastrointestinal tract, thereby increasing gastrointestinal motility and improving gastrointestinal symptoms in patients with functional dyspepsia, without affecting gastric acid secretion. Usage and precautions: Mosapride 5mg Tid. Mosapride has no affinity with dopamine D2, 5-HT4 and 5-HT2 receptors on the synaptic membrane of the brain, thus there are no extrapyramidal side effects caused by the blockage of these receptors. adverse reactions mainly manifest as diarrhea, abdominal pain, dry mouth, rash and lethargy, dizziness, etc. Occasionally, eosinophilia, elevated triglycerides and elevated ghrelin (GOT), ghrelin (GPT), alkaline phosphatase (AKP), γ-glutamyl transpeptidase (GGT) 3, acid suppressants chronic gastritis patients gastric acid can be high or low, the application of acid suppressants can improve the pH value of the stomach, reduce the damage of H+ on the gastric mucosa, that is, the degree of H+ anti-dispersion, for the gastric mucosa inflammation repair to create (1) H2 receptor antagonism (1) H2 receptor antagonists include cimetidine, ranitidine, famotidine, nizatidine and so on. All of them can inhibit gastric acid secretion from mural cells by competitively antagonizing the binding of histamine to H2 receptors. Cimetidine, ranitidine and famotidine have strong inhibition of pepsin secretion and increase the blood flow of gastric mucosa. Usage: Cimetidine 400mg Bid; Ranitidine 150mg Bid; Famotidine 20mg Bid; Nizatidine 150mg Bid. (2) Proton pump inhibitor PPI irreversibly binds to the sulfhydryl group of H+-K+-ATPase (also known as proton pump) in the secretory membrane of mural cells through disulfide bond, generating a complex of sulfenamide and proton pump, thus inhibiting the enzyme activity and blocking gastric acid secretion. It inhibits the activity of the enzyme and blocks the last link of gastric acid secretion, and therefore has a strong and long-lasting inhibitory effect on gastric acid secretion caused by various reasons. The inhibitory effect is dose-dependent and has an effect on both basal and stimulated gastric acid secretion; on the other hand, PPI can inhibit the growth of Helicobacter pylori. Therefore, proton pump inhibitors can be considered for patients with severe gastric acidity or gastritis with erosion and bleeding. Commonly used representative drugs: omeprazole, lansoprazole, pantoprazole, rabeprazole, esomeprazole. Generally use standard dose, once a day more can achieve better therapeutic effect. 4. Hp eradication therapy: Hp-positive active gastritis, Hp should be eradicated (see the section on peptic ulcer for specific usage). 5, other treatment: (1) age-related atrophy and intestinalization; nutritive drugs for gastric mucosa, such as: carotene, folic acid, zinc, VitE, etc. (2) For gastric mucosal intestinal and atypical hyperplasia, vitamin C, E and folic acid are given, and regular endoscopic follow-up is performed. Chronic atrophic gastritis with severe heterogeneous hyperplasia is mostly considered to be precancerous at present, and it is advocated that surgical treatment should be considered. (3) Treatment of autoimmune gastritis: No special, VitB12 can be injected in case of pernicious anemia. Dilute hydrochloric acid and digestive enzymes can be given to patients with poor digestive function.