Drug treatment of bile reflux gastritis Zhuang Qingping, chief physician of the First People's Hospital of Wuxi City, Jiangsu Province, recently saw stomach problems in two hospitals, and both hospitals conducted gastroscopy for him. One examination report is bile reflux gastritis, and the other report is chronic superficial gastritis with bile reflux. So, he asked me if these two gastroscopy reports were the same thing. What are the characteristics of bile reflux gastritis? What effective drugs can be used? Helicobacter pylori infection, autoimmune mechanism and genetic factors and bile reflux are considered as the three main causes of chronic gastritis, but in recent years, gastritis caused by bile reflux has attracted more and more attention. Specifically, bile reflux is duodenal juice reflux, which flows through pylorus and enters the gastric antrum. The pylorus is the outlet of the stomach, and the pyloric sphincter is formed by the thickening of the circular muscles of the stomach. Its contraction and relaxation act as a "valve", so that the contents of the stomach (chyme) can smoothly enter the duodenum through it and prevent duodenal juice from flowing back into the stomach. Under normal circumstances, a small amount of duodenal juice sometimes flows back into the stomach during digestion. Because the reflux time is short and the reflux flow is small, it will not damage the normal barrier function of gastric mucosa, which belongs to "physiological reflux" However, due to the dysfunction of pyloric sphincter, duodenal juice often flows back into the stomach in large quantities, and the normal barrier function of mucosa can't bear it, which gradually causes mucosal damage such as inflammation, erosion, bleeding and changes in cell reactivity, which is called "bile reflux gastritis". Duodenal fluid contains bile, intestinal fluid and pancreatic fluid. Cholic acid in bile is the main damage substance of gastric mucosa, and trypsin and lysolecithin are also important damage factors. If the degree of reflux is serious, the reflux fluid can cross the lower esophageal sphincter and retrograde into the esophagus, which will aggravate the damage of esophageal mucosa together with the reflux gastric juice and cause "reflux esophagitis" in time. There are two types of bile reflux gastritis: primary and secondary. Level 2 has been known for a long time. It was recognized more than a century ago that one of the complications of subtotal gastrectomy can cause reflux gastritis. Other diseases that can cause secondary bile reflux gastritis, such as cirrhosis (especially portal hypertension), biliary tract diseases (chronic cholecystitis, gallstones, after cholecystectomy), diabetes, etc. Bile reflux gastritis is primary, which originates from primary pyloric dysfunction (pyloric sphincter relaxation or prolonged opening time), and the related pathogenic factors are still under in-depth study. As we all know, imbalance of gastrointestinal hormone secretion is one of the important pathogenesis. Experiments show that when gastrin (secreted by gastric antrum) is excessively secreted, while pancreatin and cholecystokinin (both secreted by duodenum) are relatively or absolutely reduced, the tension of pyloric sphincter is reduced, so that duodenal juice can freely return to the stomach. Some life factors and bad habits, such as excessive smoking, drinking, mood swings, irregular life, especially frequent and long nightlife, can cause the above-mentioned gastrointestinal hormone secretion disorder, thus leading to pyloric dysfunction and bile reflux. The symptoms caused by bile reflux gastritis vary in severity and lack specificity. Common in the upper abdomen and middle abdomen, with fullness discomfort, belching, acid vomiting, etc. It can also be similar to peptic ulcer-like pain. Severe cases often vomit, and vomit often contains bile. A few severe patients may have upper gastrointestinal bleeding (black stool or hematemesis), and some patients have no obvious symptoms. Therefore, the diagnosis of this disease mainly depends on gastroscopy, and bile reflux can be directly observed under the microscope, and gastric mucus is dyed yellow. However, mechanical stimulation such as endoscopic insertion can also cause duodenal bile reflux, leading to false positive results. Because bile reflux often occurs intermittently, there is no reflux during gastroscopy observation, and false negative results can appear again. Therefore, seeing bile reflux during microscopic examination does not mean bile reflux gastritis. The diagnosis of the latter should be combined with the unique pathological changes, medical history and clinical manifestations of gastric mucosa. The drug treatment of bile reflux gastritis is based on the above pathogenesis: (1) weakening the attack of cholic acid on gastric mucosa. At present, aluminum magnesium carbonate (Daxi, Trsek) is widely used, which can continuously bind cholic acid in the stomach, prevent cholic acid and lysolecithin from damaging the gastric mucosa, and neutralize gastric acid. Sucralfate can also be combined with cholic acid and lysolecithin, which is a cheap and suitable drug. Sphingosine (a strongly basic anion exchange resin) is rarely used because of its strong binding with cholic acid and many side effects. Ursodeoxycholic acid can inhibit the synthesis of cholic acid, thus reducing gastric mucosal injury, but it is not widely used in practice. (2) Strengthen the control function of pylorus. The application of gastrointestinal motility drugs, such as modine, cisapride and mosapride, can enhance the tension of pylorus and lower esophageal sphincter, accelerate gastric emptying and inhibit duodenal juice reflux. The acceleration of gastric emptying can also reduce the secretion of bile and pancreatic juice. (3) Inhibit gastric acid secretion and reduce the acidity in the stomach. Gastric acid is recognized as a gastric mucosal injury factor. On the basis of bile acid damage to gastric mucosa, gastric acid also plays an "accomplice" role. Therefore, acid inhibitors such as omeprazole and rabeprazole can be added, and cheap ranitidine and famotidine can also be selected, but the effect is poor. (4) Mucosal protective agent. The above aluminum magnesium carbonate and sucralfate are good mucosal protective agents. In addition, you can also choose bismuth preparations such as Dele and Weimin, as well as Maizilin -S and Smecta.