Biliary reflux gastritis, also known as alkaline reflux gastritis, is a chronic inflammation of the gastric mucosa caused by dysfunction of the pyloric sphincter or surgery to reduce the function of the pylorus, resulting in the reflux of duodenal contents containing bile and pancreatic juice into the stomach, which, under the action of gastric acid, damages the gastric mucosal barrier and causes increased H+ diffusion. The definite diagnosis mainly relies on gastroscopy and and gastric aspirate measurement, and isotope measurement can understand the degree of reflux. Disease description: Bile reflux gastritis is a special type of chronic gastritis, commonly seen after gastrectomy and gastrointestinal anastomosis, with an overall incidence of about 5%, with the incidence after Billroth II gastrectomy being 2 to 3 times higher than that of Billroth I. Under normal physiological conditions, duodenogastric reflux exists in the organism, and the reflux does not cause injury to the gastric mucosa. However, in patients with bile reflux gastritis, due to impaired gastric-pyloric-duodenal motility, duodenal contents (such as bile acids and bile salts) reflux into the stomach and, under the action of gastric acid, destroy the gastric mucosal barrier, causing H+ reperfusion into the epithelium, resulting in chronic inflammation, erosion and even ulceration of the gastric mucosa, followed by a series of manifestations such as epigastric pain, vomiting of bile, bloating and weight loss. Biliary reflux gastritis can be divided into primary biliary reflux gastritis and secondary biliary reflux gastritis: the former is non-surgical gastric occurring in excess duodenal fluid reflux; the latter is gastric bile reflux occurring after gastric pylorus surgery or gallbladder removal. Long-term bile reflux can lead to esophagitis, erosive, proliferative, active inflammation of the gastric mucosa, gastric ulcers, and even contribute to the development of gastric cancer. Causes and mechanisms: Gastric-pyloric-duodenal dysmotility is considered to be the main pathogenesis of the disease. The increase in duodenal retroperistalsis caused by dysmotility, the weakening of pyloric closure and delayed gastric emptying can lead to excessive regurgitation of duodenal contents into the stomach. 1, Duodenogastric reflux mechanism Duodenogastric reflux is a physiological phenomenon of the body, but excessive occurrence will cause damage to the gastric mucosa. Duodenogastric reflux occurs when there is retroperistalsis in the duodenum, which coincides with the opening of the pylorus. Sometimes duodenal retroperistalsis is very strong, and if there is a strong sinus contraction. It can also prevent the occurrence of duodenogastric reflux. Any factors that lead to gastrointestinal motility disorders and anatomical abnormalities can cause pathological duodenogastric reflux to occur. 2, pathogenic role of duodenogastric reflux Bile acid is the main component of mucosal damage caused by duodenal reflux fluid, which has a significant destructive effect on the mucosal barrier. The invasiveness of juice acid on gastric mucosa is enhanced in acidic environment, and its joint action with digestive enzymes and other components can lead to changes in mucosal cells and tissue structure, while weakening the multiple protective mechanisms of gastric mucosa and promoting the action of other damage factors such as gastric acid and H. pylori. 3, H. pylori infection H. pylori infection causes gastric mucosal inflammation, bile reflux gastritis can coexist with HP infection, HP infection and bile reflux both related to mucosal damage, which may cause bile reflux by increasing gastrin release, thus affecting gastroduodenal dynamics. 4, other causes: such as primary pyloric sphincter dysfunction can make the pylorus open for a longer period of time, pylorus relaxation or take a continuous open state, so that the duodenal contents reflux into the stomach, causing the occurrence of duodenogastric reflux; such as abnormal levels of gastrointestinal neuropeptides and hormones can lead to disorders in the movement of the gastrointestinal tract and lead to the occurrence of duodenogastric reflux. Pathophysiology: Bile reflux gastritis manifests under the naked eye as diffuse erythema, congestion, and edema of the gastric mucosa; bile spots are seen attached to the wall, erosion and bleeding, and the lesions are most obvious at the gastric sinus near the pylorus. Histologically, the gastric mucosal layer may show vascular congestion and dilatation and inflammatory cell infiltration, and the lamina propria may be edematous; the epithelium of the gastric notch may show hyperplasia and intestinal epithelial metaplasia, which may be accompanied by glandular atrophy; the mucosal capillaries are congested and dilated or bleeding. Clinical manifestations: The main manifestations are abdominal fullness and discomfort, persistent burning sensation in the upper and middle abdomen, and also retrosternal pain, which may be aggravated after meals and aggravated by alkaline drugs. It may be accompanied by abdominal distension, belching, heartburn, acid reflux, nausea, vomiting, intestinal tinnitus, poor bowel movement, loss of appetite, and weight loss. Bilious vomiting is a characteristic manifestation. Due to impaired gastric emptying, vomiting usually occurs at night or in the middle of the night and may be accompanied by small amounts of food or blood. The diagnosis of bile reflux gastritis is mainly based on gastroscopy and gastric aspirate determination, and isotope determination can understand the degree of reflux. Gastroscopy: Bile reflux can be seen directly under the endoscope, and the gastric mucosa shows diffuse congestion with varying degrees of edema or erosion of the mucosal folds. Green retained fluid is seen in the gastric lumen, the pyloric opening is flaccid or in an open fixed state, and yellow foam is seen to reflux into the stomach during duodenal peristalsis. Endoscopic bile reflux can be divided into 3 degrees: degree I for the amount of yellow foam intermittently gushing out from the pyloric opening and/or mucus lake in pale yellow; degree II for yellow foam gushing out from the pyloric opening and/or mucus lake in yellow-green; degree III for frequent outflow of yellow liquid from the pyloric opening and/or persistent ejection or the stomach covered with yellow-green mucus. 2, gastric aspirate determination: by inserting a gastric tube from the patient’s nasal cavity to reach the gastric cavity, followed by aspiration of fasting and postprandial gastric juice, to determine the bile acid content, if the fasting basal gastric acid secretion <3.5mmol/h and bile acid exceeds 30ug/ml, then the diagnosis of bile reflux gastritis is confirmed. 3, Isotope determination: By intravenous injection of 2mC i 99m T c-butyliminodiacetic acid, the liver, gallbladder and gastric region were observed to determine the index of gastrointestinal reflux. The degree of gastrointestinal reflux can be understood by testing the isotope content in the stomach. Drug treatment 1, pro-gastric motility drugs: by promoting gastric emptying, reducing the residence time of bile in the stomach and promoting the emptying of refluxed material. Commonly used drugs include metoclopramide (gastric complex), domperidone (morpholine), mosapride (new lona), etc. Metoclopramide mainly acts on the gastrointestinal tract and the central nervous system, and it can act on the medullary emetic chemosensory area by blocking dopamine receptors. It has a central antiemetic effect. It enhances gastric peristalsis, promotes gastric emptying and dilation of the pylorus and duodenum, and accelerates the passage of food; domperidone is a dopamine receptor antagonist with peripheral blocking effects, promotes gastric emptying, and improves sinoduodenal coordination; mosapride is a selective 5-HT receptor agonist. By agonizing the 5-HT receptors in the myenteric plexus, it increases the release of acetylcholine from the nerve endings, thus promoting gastric emptying. 2, combined with bile salts drugs: such as Daxi (aluminum magnesium carbonate), by combining with bile acid and lysophosphatidylcholine, and then reduce the bile salt damage to the gastric mucosa, the effect on bile reflux gastritis is obvious, for the main clinical use; such as anion exchange resin (kauai enamine), after oral administration release of chloride ions, combined with bile acid, the formation of insoluble, non-absorbable complex, accelerate bile salt and fecal excretion, reduce damage to the gastric mucosa. 3, inhibit gastric acid drugs: gastric acid and bile have a superimposed effect on the gastric mucosa damage is strong, acid suppressants are also effective for bile reflux. Commonly used acid inhibitors are mainly H2 receptor blockers (H2RA) and proton pump inhibitors (PPI). The former can prevent the combination of histamine and its H2 receptor, so that the mural cells secrete less gastric acid, commonly used drugs include cimetidine, ranitidine, famotidine; the latter can prevent intracytoplasmic H-K exchange, reducing H excretion, its acid-suppressing effect is much better than H2 receptor blockers. Commonly used drugs include omeprazole, lansoprazole, rabeprazopam, tolazol, and esomeprazole, the course of treatment is generally 2 weeks. 4, anti-H. pylori treatment: H. pylori infection can cause inflammation of the gastric mucosa, bile reflux gastritis can coexist with H. pylori infection. Therefore, the treatment of bile reflux gastritis combined with HP infection, in the routine application of acid suppressants, gastric mucosal protective agents and gastric power drugs at the same time. The eradication of H. pylori should also be considered first. This is not only beneficial to the healing of the disease, but also can reduce the possibility of inducing cancer. Surgical treatment: mainly for those with severe symptoms for which medical treatment is ineffective, commonly used procedures are Roux-en-Y surgery or biliary shunt. Prognosis: The prognosis is general. Long-term bile reflux can lead to esophagitis, gastric mucosal erosion, hyperplasia, active inflammation, gastric ulcer, and even gastric cancer. Dietary attention: pay attention to dietary hygiene, avoid strong alcohol, strong tea and strong coffee, eat hot and cold items in moderation, consume less rough and spicy food that can damage the gastric mucosa, and avoid overeating. Do not eat in emotional or depression and other adverse psychological states, so as to avoid emotional changes will affect the secretion of digestive juices, eating should pay attention to a small number of meals, low-fat diet, high fat can make the small intestine mucosa release cholecystokinin, gastrointestinal contents more easily reflux, and thus increase the frequency of reflux symptoms. Overweight people should lose weight, because the increased abdominal pressure in overweight people can promote gastric reflux, especially in the prone position, so weight should be actively reduced to improve the reflux symptoms. In addition, activities that increase intra-abdominal pressure should be minimized, such as excessive bending, wearing tight-fitting clothes and pants, and tightening the belt. Complications: The disease can be complicated by esophageal strictures, bleeding, and ulcers. Chronic pharyngitis, chronic vocal fold inflammation and tracheitis, known clinically as Delahunty's syndrome, can result from erosion of the pharynx, vocal folds and trachea by the refluxed gastric juice. Gastric reflux and aspiration into the respiratory tract can lead to aspiration pneumonia. Expert opinion: Long-term and severe bile reflux gastritis can increase the occurrence of gastric cancer, so patients with bile reflux gastritis should pay enough attention to it. In addition to actively cooperating with medication and surgery, patients should pay more attention to the adjustment of diet and lifestyle. Through a healthy diet and good lifestyle habits, the attack of bile reflux gastritis can be prevented and controlled to the greatest extent.