Bile reflux gastritis

　　(I)Etiology

　　1.Bile has a greater damaging effect on gastric mucosa in an acidic medium, especially under ischemic conditions.

　　2.Bile, pancreatic juice, and duodenal juice containing lysophosphatidylcholine have the greatest destructive effect on gastric mucosa.

　　3.In patients with gastric ulcer, those with a higher concentration of bile in the stomach, the growth of Gram-negative aerobic bacteria in gastrointestinal aspiration fluid increases.

　　4.In patients with clinical symptoms, the concentration of deoxycholic acid in gastric juice increases.

　　5.Delayed gastric emptying prolongs the contact time between bile and gastric mucosa.

　　(II)Pathogenesis

　　1.The mechanism of DGR: The physiological study of gastric motility proves that the pylorus is mostly in an open state, and the small amount of duodenal reflux into the stomach is not enough to cause symptoms or damage the gastric mucosa, which is called physiological DGR. The occurrence of large amounts of DGR is common in the following situations:

　　(1)Postoperative DGR after gastric surgery: The incidence of postoperative DGR of the stomach is 5% to 60%. Due to the damage to the normal anatomical structure and physiological function of the pylorus, the anti-DGR barrier function of the pylorus is lost after surgery, causing excessive alkaline intestinal juice containing bile components to reflux into the stomach, and leading to residual gastritis and bile vomiting. Griffiths reported 71 cases of postoperative stomach, 41.9% showed bile reflux, 61.5% had diffuse gastritis. Bile reflux from the duodenum or small intestine to the stomach after gastric surgery, since part of the surgery is a gastric jejunostomy, it should be accurately called small intestinal-gastric reflux (entro-gastric reflux). The severity of small intestinal-gastric reflux is closely related to the surgical method, and is arranged in order of severity as follows:

　　①Pyloroplasty.

　　②Vagotomy and pyloroplasty.

　　③Gastric jejunostomy.

　　④Billroth Ⅰ type gastric resection.

　　⑤ Billroth II gastric resection.

　　(2) Primary pyloric dysfunction: Modern research on gastrointestinal motility function has proven that some pathological DGR is not due to post-gastric surgery, but originates from the defect of the pylorus itself, such as pyloric sphincter dysfunction, such as prolonged pyloric opening time, dysfunction of the pyloric hypertension zone, and other factors lead to a large amount of duodenal content reflux into the stomach.

　　In 1973, Fisher measured the pressure of the pyloric hypertension zone using the perfusion method as (5.3±0.5) mmHg. Zhang Jinkun and Luo Jinyan in China, among others, also confirmed the existence of the pyloric hypertension zone using the intracavitary metallic sensor method. People believe that the gastric duodenal barrier pressure (GDBP = pyloric pressure - duodenal pressure) has an anti-reflux effect. When GDBP decreases, it causes DGR to occur. Chinese reports show that the GDBP of DGR patients is lower than that of the normal control group.

　　Animal experiments have observed that during the interdigestive migrating motor complex (MMC) II phase, due to atypical segmental contractions accompanied by DGR, DCR also occurs in humans during the MMC II phase. The mechanism may be:

　　① During the MMC II phase, bile and pancreatic secretions accumulate in the duodenum.

　　② Due to the small regular movement and pressure changes in the MMC II phase, a certain pressure gradient is produced, which increases the intraduodenal pressure and causes gastrointestinal reflux.

　　(3) Delayed gastric emptying: Whether idiopathic or secondary delayed gastric emptying (such as idiopathic gastroparesis, diabetic gastroparesis), due to the dysfunction of gastric peristalsis and the pylorus, it leads to a decrease in GDBP and a large amount of duodenal reflux. Once DGR occurs, it can further slow down gastric emptying, so some people believe that delayed gastric emptying and DGR can be mutually causal (delayed gastric emptying DGR).

　　(4) Liver and biliary diseases: Patients with liver cirrhosis and portal hypertension have a high incidence of DGR. The mechanism is believed to be due to circulatory disorders caused by portal hypertension, in addition to secondary hypergastrinemia, which inhibits the regulation of cholecystokinin and secretin on the pyloric sphincter and Oddi sphincter, causing a decrease in the tone of the latter two, and the reflux of bile and pancreatic juice into the stomach.

　　Many biliary diseases (such as cholecystitis, gallstones, and post-cholecystectomy) are accompanied by significant DGR phenomena. Due to biliary diseases, the function of gallbladder reserve and bile concentration is reduced and disappeared, causing bile to flow continuously from the bile duct into the duodenum and reflux into the stomach through the pylorus.

　　Autonomic nervous dysfunction, excessive smoking, drinking, emotional fluctuations, changes in life routine, and other conditions can cause disordered secretion of gastrointestinal hormones, and lead to retrograde peristalsis of the antrum and duodenum and a decrease in the tone of the pylorus, resulting in unbalanced motility of the stomach and duodenum, providing the necessary pressure gradient for the reflux of substances through the pylorus, and promoting the occurrence of DGR.

　　2. Pathogenesis of bile reflux gastritis (BRG)

　　Gastric surgery, such as subtotal gastrectomy, generally leads to residual gastritis or bile reflux gastritis (BRG) due to bile reflux several months or years later, and symptoms such as upper abdominal pain or vomiting bile may occur.

　　A large number of animal experiments and clinical observations have proven that the reflux of bile and duodenal contents into the stomach can cause gastritis. It has been found that the extent and severity of gastritis are linearly related to the degree of bile reflux and are related to the reflux components. Bile acids and lysophosphatidylcholine are the main components that damage the gastric mucosa. Bile salts can dissolve phospholipids and cholesterol from the gastric mucosa and interfere with the energy metabolism of gastric mucosal epithelial cells, causing lysosomes to rupture. At the same time, they have a clearing effect on the mucus on the surface of the gastric mucosa, damaging the gastric mucosal barrier, increasing the reverse diffusion of H+, causing mast cells to release histamine, leading to the occurrence of gastritis. A large number of DGR not only directly damage the gastric mucosa and cause gastritis but are also related to the occurrence of gastric ulcers. Rhodes J et al. (1972) found that the DGR of patients with gastric ulcers is higher than that of normal people. The mechanism may be that cytotoxic bile salts and trypsin first damage the gastric mucosa in excess, followed by proliferative changes, intestinal metaplasia, and the formation of ulcers. In addition, DGR can reflux into the esophagus at the same time, playing an important role in the pathogenesis of reflux esophagitis and Barrett's esophagus, known as duodenogastric-oesophageal reflux (DGER). Some research reports suggest that DGR is also related to the occurrence of esophageal cancer and residual gastric cancer.

　　Patients with bile reflux gastritis often have symptoms such as anemia, weight loss, chronic diarrhea, insomnia with frequent dreams, palpitations, and other symptoms of neurosis, which seriously affect the daily life of patients and hinder their health. It is necessary to treat it in time.

　　Typical symptoms of bile reflux gastritis:

　　Symptoms such as upper abdominal pain, chest pain after overeating, bloating, decreased appetite, nausea and vomiting, diarrhea, weight loss, and weight loss.

　　Patients often complain of persistent pain in the upper middle abdomen, which worsens after meals, and antacids are ineffective, even exacerbating symptoms. A few patients may present with pain behind the sternum, a feeling of indigestion, often vomiting 'bitter water' or bile in the evening or early morning on an empty stomach, sometimes mixed with food. The vomiting does not relieve the symptoms. Patients often have anemia, weight loss, chronic diarrhea, and insomnia with frequent dreams, palpitations, and other symptoms of neurosis. The physical signs are often manifested as pain in the upper abdomen.

　　Prevention of bile reflux gastritis

　　1. If DGR and BRG are caused by post-gastric surgery, the choice of surgical method is very important.

　　2. If the DGR is caused by autonomic nervous dysfunction, excessive smoking, drinking, and other changes in life habits leading to the secretion disorder of gastrointestinal hormones, it is very important to strengthen physical exercise and change the lifestyle.

　　Laboratory examination
　　1. Monitoring of gastric pH value
　　2. Determination of sodium in gastric juice
　　3. Determination of bile acid in fasting gastric juice
　　4. Determination of trace bilirubin in 24h bile
　　Imaging examination
　　1. Gastroscopy and histological examination
　　2. Early diagnosis by radiological examination
　　3. Gastrointestinal pressure measurement
　　4. Gastric acid perfusion irritation test
　　5.核素检查
　　5. Radioisotope Examination

　　Dietary taboos for patients with bile reflux gastritis

　　Dietary health care for bile reflux gastritis

　　Specific dietary advice needs to be consulted with a doctor according to symptoms, ensure a reasonable diet, and ensure a comprehensive and balanced nutrition.

Conventional methods of Western medicine for the treatment of bile reflux gastritis

Precautions before the treatment of bile reflux gastritis

(First) Drug Treatment Drug treatment should be adopted first, and surgical treatment should be considered only when drug treatment fails and the symptoms are severe.

Cholestyramine is an alkaline anion exchange resin that can combine with bile salts in the stomach and accelerate their excretion. Initially, 4g is taken one hour after meals, and an additional dose is taken before bedtime. It usually takes effect after 1-2 weeks of taking the medicine, and then the dosage is gradually reduced. Lipid-soluble vitamins should be supplemented at the same time. If there is no effect after 3 months of treatment, it is considered a treatment failure.

Metoclopramide (Stomach Reglan) can promote the contraction of the stomach cardia and the proximal small intestine, accelerate gastric emptying, alleviate the symptoms of patients with gastric emptying disorders, and can also further reduce the secretion of bile and pancreatic juice, relieve the symptoms of reflux gastritis.

(Second) Surgical Treatment There are basically four types of surgical methods.

1. Change to Billroth I Technique If the original Billroth II gastric resection is changed to Billroth I, about half of the patients' symptoms can be improved.

2. Roux-en-Y Surgery For those who were originally Billroth II surgery, the input segment at the anastomosis is cut off, and the proximal incision end is anastomosed to the output loop (see Figure 1).

Figure 1 Roux-en-Y Gastric Jejunum Anastomosis

3. Jejunum Interposition Surgery For those who were originally Billroth I gastric resection, a segment of about 20cm of jejunum is placed in the middle of the stomach duodenum anastomosis, with an efficacy rate of 75％.

4. Tanner Surgery Is suitable for those who were originally Billroth II surgery, cut the jejunum input loop, and connect the distal incision end with the jejunum output loop to form a loop. The proximal incision end is anastomosed to the jejunum 50cm away from the original stomach jejunum anastomosis (see Figure 2).

Figure 2 Tanner Surgery

In addition, to prevent the occurrence of anastomotic ulcer, vagotomy can be considered.