Biliary reflux gastritis is a specific type of chronic gastritis caused by the reflux of bile from the duodenum into the stomach. The bile refluxes into the gastric sinus, which is closest to the pyloric hilum (the place where food passes through to connect the stomach to the duodenum), causing damage to the mucosa there. Clinical manifestations The main symptoms of the disease are a feeling of fullness or discomfort in the upper abdomen, with vague or severe pain, often in periodic episodes, and may be accompanied by abdominal distention, belching (burping), acid reflux, heartburn, nausea, vomiting, loss of appetite and emaciation. Gastroscopy shows that bile is constantly pouring into the stomach from the pylorus, and the gastric mucosa (especially the mucosa of the gastric sinus) is obviously edematous, congested, rough, and bleeds easily when touched, with a dirty surface and yellow-green bile. Secondly, the nuclear test is to label bile with 99mTc and secrete it through the liver to the duodenum to see if there is reflux, and 24-hour bile monitoring in the stomach is also a reliable method to determine whether there is bile reflux. Under normal circumstances, the pyloric opening is contracted and closed. When food in the stomach is discharged into the duodenum by gastric peristalsis, the pyloric opening is developed diastically, and after the food is emptied, the pyloric opening is contracted and closed again, thus preventing bile reflux into the stomach. After partial gastrectomy, vagotomy and pyloroplasty, gastrointestinal anastomosis, gallbladder removal, congenital pyloric portal closure, etc., the “gatekeeper” role of the pyloric portal is destroyed, and bile reflux can occur. The incidence of this disease increases after cholecystectomy (60% of patients with this disease have a history of cholecystectomy), which is related to the uninterrupted flow of bile into the duodenum 24 hours a day (when the gallbladder is normal, bile enters the duodenum regularly after meals). Treatment Treatment of bile reflux gastritis is currently very difficult and cannot be completely cured, and medication discontinuation does not prevent the occurrence of bile reflux or damage to the gastric mucosa from bile. Current therapeutic drugs include complex bile acids, gastrointestinal motility drugs, gastric mucosal protective agents, acid suppressants, etc. 1, complexed bile acid: there are anion exchange resins, and its representative drugs are abbreviated bile amine and colestipol. Mainly combined with bile acid and excreted through the intestinal feces, blocking the enterohepatic circulation of bile acid, affecting the absorption of fat and fat-soluble vitamins; magnesium aluminum carbonate (Daxi), which has the ability to bind bile acid and lysolecithin in the stomach, the binding rate of 100% in an acidic environment, can reduce the stimulation of bile on the stomach. 2, pro-gastrointestinal dynamics drugs: can enhance the peristalsis of the esophagus and stomach, improve gastrointestinal emptying and coordinated contraction of the gastric sinus duodenum, reduce the residence time of bile in the stomach, such as domperidone and mosapride. 3, gastric mucosa protective agents: there are magnesium aluminum carbonate, aluminum thioglycollate, bismuth potassium citrate, etc., the stomach to form a protective film to prevent gastric acid and pepsin damage to the gastric mucosa, inhibit pepsin activity, increase prostaglandin synthesis. 4, acid inhibitors: there are H2 receptor blockers and proton pump inhibitors, such as famotidine, omeprazole, etc., to inhibit acid secretion, can reduce the effect of bile acid on gastric damage.