Bile reflux gast ritis (BRG), also known as duodenogastric reflux disease, is a chronic inflammation of the gastric mucosa caused by the reflux of duodenal contents containing bile and pancreatic juice into the stomach due to the dysfunction of the pyloric sphincter or surgery to reduce the function of the pylorus. The main causative factor is bile, which mainly manifests as a series of syndromes such as epigastric pain, vomiting of bile, abdominal distension and weight loss. Many patients think that “bitter mouth” is related to bile reflux because people think that bile is bitter, but in fact, unless there is very serious gastroesophageal reflux, bile may reflux to the pharynx with gastric contents, otherwise it is almost impossible for bile to reach the oral cavity. The symptom of “bitter mouth” is more often associated with improper diet, insomnia, anxiety, etc. Pathogenesis: Biliary reflux gastritis is often divided into two categories: non-surgical gastric reflux of excessive duodenal fluid, called primary biliary reflux gastritis, and coordinated gastric-pyloric-duodenal dysmotility is thought to be the main pathogenesis of primary biliary reflux gastritis. Gastritis caused by excessive bile reflux that occurs after pyloric surgery or cholecystectomy is called secondary biliary reflux gastritis. Bile acid and bile salts in bile are fat-soluble substances that can dissolve gastric mucus and thus lose the barrier function; they can also lower the acidity in the stomach, increase gastrin, relax the pyloric sphincter, and aggravate bile reflux. Lecithin in bile interacts with phospholipase A in pancreatic juice to form hemolysed lecithin, which has a stronger mucosal damaging effect. Bile reflux causes a low-acid or acid-free environment in the stomach, which allows bacterial overgrowth in the stomach, which allows bile acids to be transformed into more toxic free bile acids, causing damage to the biochemical integrity of the gastric mucosa, congestion and edema of the gastric mucosa, persistent epigastric distension or burning sensation with nausea and vomiting, which is not easily relieved by eating or taking antacids. Diagnosis: 1. Endoscopy The gastroscopic diagnostic criteria for bile reflux gastritis are: a yellow or yellow-green bile-like pool of mucus is seen on the gastroscope, bile stasis is seen on the gastric mucosa, and the mucosa is congested, edematous, brittle or eroded, and beefy red. Gastroscopy is visual in nature, but is prone to false positive results due to the significant nausea response in most patients. In general, if this is the case with painless gastroscopy, or if the bile adhering to the gastric wall is thick and not easily flushed away, and if the gastric mucosa is rough and uneven, then the patient may have long-term chronic bile reflux. In addition, as suggested by Kellosalo et al, the color of gastric mucus lake is divided into 0, 1, 2 and 3 levels of reflux based on the color of the gastric mucus from clear, light, medium to dark yellow or yellow-green, which can exclude bile reflux in some cases due to stimulation of the insertion, etc. and significantly improve the accuracy of gastroscopy diagnosis. 2, pathological examination Bile reflux gastritis gastric sinus mucosal tissue has special pathological changes, manifesting as hyperplasia of gastric pits, congestion of the lamina propria, vasodilation and mucosal muscle hyperplasia, while inflammatory cell infiltration is relatively light. Treatment: Treatment of bile reflux gastritis on the one hand should be combined with bile acids to reduce the damaging effects of reflux; on the other hand, gastrointestinal dynamics should be improved to promote coordinated gastroduodenal movement to reduce the occurrence of duodenogastric reflux. Current treatment includes gastric motility agents (Mosapride or Itopride) + bile adsorption mucosal protective agents (Simethicone and magnesium aluminum carbonate) + acid suppressants (Rabeprazole, Omeprazole, Pantoprazole, Esomeprazole, etc.), psychotherapy, surgical treatment, etc. In addition, dietary habits are also critical. (1) Food selection: low-fat, easily digestible foods should be the mainstay to avoid stimulating increased bile secretion. (2) Form good dietary habits: Patients should pay attention to regular diet and eat three meals on time, because it is easy to cause reflux after eating, so it is not advisable to rest flat and interact vigorously immediately after eating. (3) should not eat too much before bedtime (4) lose weight (excessive obesity will increase abdominal pressure and contribute to reflux, so the intake of high-fat foods that promote reflux should be avoided and weight should be reduced) (5) raise the head of the bed 10-15 cm (this is very important for reflux at night when lying down, using gravity to remove harmful substances in the esophagus) (6) avoid various actions and positions that increase abdominal pressure for a long time in life (including wearing tight clothing and tight belts). (7) Stop smoking and drinking; (8) Relax your mind.