Duodenogastric reflux and bile reflux gastritis
Introduction
Brief introduction of duodenogastric reflux and bile reflux gastritis Duodenal contents bile, pancreatic enzymes and alkaline intestinal contents flow back into the stomach called duodenogastric reflux (DGR). Alkaline reflux or bile reflux is a common pathological phenomenon. In the past, it was believed that some degree of DGR helped to buffer acidity in the stomach. Excessive DGR causes gastritis due to the destruction of the gastric mucosal barrier by duodenal bile contents. basic knowledge The proportion of illness: 0.035% Susceptible people: no special people Mode of infection: non-infectious Complications: anemia, diarrhea, insomnia
Cause
Duodenogastric reflux and the cause of bile reflux gastritis
(1) Causes of the disease
There are the following factors in the pathogenesis of duodenal reflux fluid:
1. Bile in the acidic medium, especially under ischemic conditions, the damage to the gastric mucosa is aggravated.
2. Bile plus pancreatic juice and duodenal juice containing lysolecithin have the greatest damage to gastric mucosa.
3. Patients with gastric ulcer, the higher the intragastric bile concentration, the increase of Gram-negative aerobic bacteria in the gastrointestinal tract.
4. In patients with clinical symptoms, the concentration of deoxycholic acid in gastric juice is increased.
5. Slow gastric emptying, prolonging the contact time of bile and gastric mucosa.
(two) pathogenesis
1. The mechanism of DGR: gastric physiology research proves that the pylorus is open for most of the time, a small amount of duodenum reflux to the stomach is insufficient to cause symptoms and damage to the gastric mucosa called physiological DGR, and the occurrence of a large number of DGR is common in the following Situation:
(1) DGR after gastric surgery: The incidence of postoperative gastric DGR is 5% to 60%. The postoperative stomach damages the normal anatomical structure and physiological function of the pylorus, leading to the loss of pyloric anti-DGR barrier, resulting in excessive bile-containing components. Alkaline intestinal fluid flows back into the stomach and causes residual gastritis and bilious vomiting. Griffiths reports 7l cases of postoperative stomach, 41.9% see bile reflux, 61.5% have diffuse gastritis, and bile from the duodenum or small intestine after gastric surgery Gastric reflux, because part of the operation is gastric jejunal anastomosis, it should be called entro-gastric reflux. The severity of small intestinal reflux is obviously related to the surgical procedure. as follows:
1 pyloric angioplasty.
2 vagus nerve cutting and pyloric angioplasty.
3 gastrojejunostomy.
4 Billroth I gastrectomy.
5 Billroth II gastrectomy.
(2) Primary pyloric dysfunction: Modern gastrointestinal motor function studies have shown that some pathological DGR is not caused by postoperative gastric surgery, but is due to defects in the pylorus itself, pyloric sphincter dysfunction, such as pyloric opening time prolongation, pylorus High-pressure band dysfunction and the like cause a large amount of duodenal contents to flow back into the stomach.
In 1973, Fisher applied perfusion method to measure the pressure of pyloric high pressure zone was (5.3±0.5)mmHg. Domestic Zhang Jinkun and Luo Jinyan also confirmed the existence of pyloric high pressure band by intracavitary metal sensor method. It is considered that the gastroduodenal barrier Pressure (GDBP = pyloric pressure - duodenal pressure) has anti-reflux effect. When GDBP is decreased, it causes DGR. The gastric mucosal barrier pressure of DGR patients is lower than that of normal control group.
Animal experiments have observed that during the interdigestive migrating motor complex (MMC) phase II, atypical segmental contractions are accompanied by DGR, and human DCR also occurs in the MMCII phase. Yes:
1 In the MMCII phase, bile and pancreas are secreted and concentrated in the duodenum.
2 Due to the movement and pressure changes of the MMCII phase, a certain pressure gradient is generated to increase the internal pressure of the duodenum and cause gastrointestinal reflux.
(3) slow gastric emptying: whether it is idiopathic or secondary gastric emptying (such as idiopathic gastroparesis, diabetic gastroparesis), due to gastric motility and pyloric dysfunction, GDBP is reduced and resulting in a large number Duodenal reflux, once DGR occurs, can further slow the gastric emptying, so some people think that gastric emptying and DGR can be mutually causal (stomach emptying DGR).
(4) Hepatobiliary diseases: patients with cirrhotic portal hypertension have a higher incidence of DGR, and the mechanism is considered to be due to portal hypertension caused by circulatory disorders, combined with secondary hypergastrinemia, inhibition of cholecystokinin and promotion The regulation of pancreatic sphincter on the pyloric sphincter and Oddi sphincter causes the tension of the latter two to decrease, and the bile and pancreatic juice flow back into the stomach.
Many biliary tract disorders (cholecystitis, gallstones, cholecystectomy, etc.) are associated with significant DGR. Due to biliary tract disease, the gallbladder is stored, and the function of the concentrated bile is reduced and disappeared, resulting in a steady flow of bile from the bile duct into the fingers. Intestines, and retrograde through the pylorus into the stomach.
Autonomic dysfunction, excessive smoking, drinking, mood swings, changes in lifestyle, etc. can cause disorders of gastrointestinal hormone secretion, and cause gastric antrum, duodenal reverse peristalsis and pyloric tension drop, leading to the stomach, twelve The imbalance of the intestinal motility function provides a necessary pressure gradient for the reflux through the pylorus, which promotes the occurrence of DGR.
2. Pathogenesis of bile reflux gastritis (BRG):
Stomach surgery, such as most of the stomach resection, usually occurs after months or years of residual gastritis or bile reflux gastritis (BRG) due to bile reflux, and produces symptoms such as upper abdominal pain or vomiting bile.
A large number of animal experiments and clinical observations have shown that the reflux of bile and duodenal contents to the stomach can cause gastritis, and the extent and severity of gastritis is linearly related to the degree of bile reflux, and is related to reflux components. Acid and lysolecithin are the main components that damage the gastric mucosa. Bile salts can dissolve phospholipids and cholesterol from the gastric mucosa, interfere with the energy metabolism of the gastric epithelial cells and rupture the lysosomal membrane, and have mucus on the surface of the gastric mucosa. Clearing action, damage the gastric mucosal barrier, and increase the reverse diffusion of H, causing histamine to release histamine, leading to gastritis. A large amount of DGR not only directly damages gastritis in gastric mucosa, but also is related to the occurrence of gastric ulcer, Rhodes J et al. 1972) Patients with gastric ulcer found that the DGR is higher than that of normal people. The mechanism may be that the gastric mucosa is first damaged by the excess of cytotoxic bile salts and trypsin, followed by hyperplastic changes, intestinal metaplasia and ulceration. In addition, DGR can simultaneously reverse Inflow into the esophagus, plays an important role in the mechanism of reflux esophagitis and Barrett's esophagus, known as duodenal gastroesophageal reflux (DGER) Some studies report DGR remnant gastric cancer and esophageal cancer and is also relevant.
Prevention
Duodenogastric reflux and prevention of bile reflux gastritis
1. If DGR and BRG are caused after stomach surgery, it is very important to choose the procedure.
2. DGR, which is caused by autonomic dysfunction, excessive smoking, drinking and other changes in lifestyle, causes gastrointestinal hormone secretion disorder, which enhances physical exercise and changes lifestyle.
Complication
Duodenogastric reflux and complications of bile reflux gastritis Complications, anemia, diarrhea, insomnia
Patients often have anemia, weight loss, chronic diarrhea and insomnia, and mental symptoms such as palpitations.
Symptom
Duodenogastric reflux and bile reflux gastritis symptoms Common symptoms Gastrointestinal cold bile reflux milk color or rice soup-like chest hole pain appetite loss weight loss bloating in the upper abdomen pain after eating thoracic pain weight loss
Patients often complain of persistent pain in the upper abdomen, exacerbated after meals, antacids are ineffective, and even worse, a few patients may present with pain in the back of the chest, "not digested", often vomiting "bitter water" in the evening or early morning fasting Or bile, sometimes mixed with food, does not relieve after vomiting, patients often have anemia, weight loss, chronic diarrhea and insomnia, dreams, palpitations and other symptoms of neurosis, often manifested as pain in the upper abdomen.
Examine
Duodenogastric reflux and examination of bile reflux gastritis
Laboratory inspection
Many techniques have been used to detect and evaluate DGR, and attempts to identify physiological DGR and pathological DGR. In recent years, due to the continuous advancement and development of biomedical engineering technology, clinically, DGR can be evaluated objectively.
1. Monitoring of pH in the stomach: continuous monitoring of pH value in the stomach for 24 hours can be used as an effective method for detecting DGR. The test can be carried out under approximate physiological conditions to obtain white peony (including meals, after meals), 24 hours at night, lying position. All the data, the normal human body fasting stomach pH value is rarely > 2, eating and postprandial pH increase, the meal can increase the pH of the stomach to above 4.0, about 30 ~ 40min back to the baseline. In the latter half of the night or In the early morning, the pH value increased in a short time, and the pH value rose from the baseline to 4-6. Some people call this the pH reversal phenomenon or the alkalinization of gastric juice, which may be related to duodenogastric reflux, and some people think that it is related to vagus nerve activity. Attenuation is related to or related to low acid secretion. Domestic Gong et al. reported that the pH of fasting gastric juice in healthy people is around 2.0, there are three food-related pH values rising during the day, and spontaneous pH values from 0:40 to 4:33 in the morning. The rise may be related to duodenogastric reflux. Studies have shown that normal people also have DGR, but the duration is short, about 1h, the number of occurrences is less, <3 times / d, due to changes in individual values of pH in the stomach. Large, and many influencing factors, such as stomach acid, diet buffer, Emptying, swallowing saliva, spontaneous reflux, etc., makes it difficult to establish a suitable diagnostic criteria for DGR. So far, there is no specific, more uniform DGR diagnostic index like gastroesophageal reflux (GER) at home and abroad. The authors had 30 cases of chronic gastritis and 10 volunteers for 24h intragastric pH monitoring. The results are shown in Table 1, indicating that the DGR() has a significantly increased pH >4 or more.
2. Determination of Na in gastric juice: The concentration of Na in duodenal juice is high, and it is stable at about 146mmol/L, which is more stable than the concentration of bile in intestinal fluid (bile is intermittently discharged from the biliary tract into the intestine), and it flows back into the stomach. Na is not destroyed and inactivated by gastric acid, and has the characteristics of convenient detection. It can be used as a diagnostic indicator of DGR. It has been studied to measure the Na and cholic acid levels in the gastric cavity while monitoring the gastric pH. There is a good linear relationship. The detection of Na concentration is a simple and easy method to judge DGR. In our hospital, we have measured the fasting gastric juice Na in the DGR ( ) gastritis group (28 cases) and DGR (-) gastritis group (24 cases). The concentration of DGR( ) was (62.87±8.31) mmol/L, and that of DGR(-) was (32.18±4.67) mmol/L. The content of Na in the two groups was significantly different (P<0.01).
3. Determination of fasting gastric acid bile acid: Cholic acid is commonly found in the stomach with DGR and is not destroyed by gastric acid. It can be used as a "marker" for duodenal juice. Measuring its concentration in gastric juice is important for understanding the degree of reflux. Significance, but the stimulation of the intubation process is easy to cause artificial reflux. Even if the fasting gastric juice is taken, its bile acid content will be affected, and false positive results may occur. On the other hand, bile in the duodenal juice depends on the emptying of the gallbladder. If the bile is not excreted into the duodenum, it will cause false negative results. The 99mTc-EHIDA scan shows that the average interval of gallbladder contraction is 70min. Therefore, the gastric juice is continuously collected, and the determination of the bile acid content can improve the positive rate of DGR diagnosis. The authors used continuous gastric aspiration for 90 min, with total bile acid 100 mol/h or bile acid concentration 1000 mol/L as the standard for the diagnosis of DGR. Compared with radionuclide, the former was 80%, and the latter was 70%. .
4. Determination of trace bilirubin: 24h hour bile reflux monitor ing The main components of DGR are alkaline intestinal fluid, bile and pancreatin, etc., using bilirubin to evaluate whether there is The occurrence of DGR, physiological inhibition of pathology, the late use of optical fiber sensing technology designed by the fiboptic technique for 24-hour bile reflux monitoring (Bilitec, 2000), the peak of characteristic absorption spectrum of bilirubin At 450nm, the application of this technology can not only qualitative DGR, but also quantify the amount of bile reflux. Through the analysis of multiple parameters, it is important to evaluate bile reflux, and also to monitor the reflux of gastroesophageal bile. Commonly used in Barrett's esophagus, esophagitis with ineffective acid reflux medication, evaluation of residual gastritis after gastrectomy, etc., need to be fasted for more than 6h, intubation from the nasal cavity, the sensor is placed 5cm below the lower esophageal sphincter, into the standard meal (Limited alcohol, beverages and acidic foods, pigments, etc.) fixed catheter, wearable recorder for 24h mobile monitoring, results processed by computer software including 24h bile anti The total number of flows, the number of refluxes over 5 min, the longest reflux time and the percentage of total reflux time, etc. The technique detects bile reflux, so it is affected by the MMC phase, and in some liver diseases such as congenital constitution In the case of jaundice (Gilbert's disease and Dubin Johnson's syndrome), it is not applicable. In addition, in an acidic environment, since the bilirubin is converted into a dimer, the peak of light absorption changes from 453 nm to 400 nm, and the detected value will decrease.
Film degree exam
1. Gastroscope and histological examination: bile reflux can be directly observed under gastroscope, gastric mucosa is stained yellow, and gastric mucosal congestion and edema are granular, vascular changes are obvious, tissue is fragile or erosive, necrosis and hemorrhage , histological examination: in addition to obvious inflammatory cell infiltration, there are still small pieces of erosion, necrosis, intestinal metaplasia, dysplasia and other changes, endoscopy can understand the degree of reflux, the severity of gastritis, but within Mirror can not be quantified, and endoscopy itself can cause reflux, so there is a high false positive rate.
2. Radiological examination: Early diagnosis of DGR is by intubation method, the catheter is inserted into the duodenum, and the barium sulfate solution is injected to observe the anti-inflow of the expectorant into the stomach under fluoroscopy, and the patient's discomfort due to intubation. And the influence on the physiological function of the pylorus, and subjective color in the judgment often, so the false positive rate is higher, and this method is basically abolished today.
3. Gastrointestinal pressure measurement: Pressure of the gastric antrum, pylorus and duodenal ampulla were measured by pressure sensor or perfusion catheter. Most patients with DGR had gastric antrum, pyloric pressure decreased, and duodenal ampulla pressure increased.
4. Intragastric perfusion irritation test: When the alkaline solution (0.1N NaOH 20ml / time) in the stomach, upper abdominal pain, with or without nausea, is classified as perfusion positive, this test is sensitive, simple and easy And specific.
5. Nuclide examination: using the radionuclide scintillation diagram excreted by the bile through the liver, non-invasively measuring reflux, without mechanical stimulation and under similar physiological conditions, can accurately determine the presence or absence of reflux and reverse flow, currently Domestic and foreign scholars agree that 99mTcEHIDA radionuclide scanning technology is the "gold index" of DGR quantification, which is superior to gastroscopy and fasting bile acid determination. The sensitivity of this method is high. When the ratio of total radioactivity to intravenous injection is >1% It is positive at the time and has good reproducibility (75%), which has become a valuable research tool and clinical diagnostic tool.
However, radionuclide examination also has certain defects. Because the anatomical position of the stomach is difficult to accurately locate, the accuracy of this technique is lowered, which affects the quantitative result of DGR. The concentration of nuclide in the stomach is often difficult to represent the true contour of the stomach, especially the stomach. The sinus is more difficult to describe, and the coverage of the liver and duodenum-intestinal fistula will also affect its accuracy. Although it can be limited, the activity of these areas is often not constant, and the body activity increases when the patient is in a lying or standing position. The difficulty of judging the concentration zone, the above factors can cause diagnostic bias.
6. Ultrasound examination King: PM et al (1984) first used real-time ultrasound to detect DGR, then Hausken T et al (1991) used color Doppler ultrasound to observe the flow and reflux of gastric contents. This method represents the DGR evaluation technique. Leap, non-invasive, reproducible, and energy DGR, the specific steps are as follows: fast 1 night to take a seat, 1 liquid test meal (400ml broth or milk) in 2min, put the probe in the pylorus At the plane level, observe the antrum of the stomach, the pylorus and the proximal end of the duodenum. According to the color signal (the liquid flow is blue to the distal end and the reflux is red), the reflux is judged. The severity of the DGR can be determined according to its frequency and intensity. Evaluation, the technical shortcoming is that the current DGR can only be measured by liquid test, and at the same time, due to factors such as flatulence or abdominal fat layer thickness, it often brings some technical difficulties.
Diagnosis
Diagnosis and identification of duodenogastric reflux and bile reflux gastritis
diagnosis
If there is a clear history of gastric surgery, biliary anastomosis, typical symptoms and gastroscopy and histopathological examination, it is not difficult to diagnose DGR and BRG; if there is no history of surgery, the clinical symptoms of DGR and BRG are not specific. Diagnosis is difficult and can be assessed and diagnosed by means of ultrasonography, radionuclide technique, intragastric 24h pH monitoring or intragastric 24h bilirubin monitoring.
Differential diagnosis
1. Lymphocytic gastritis:
It is a newly confirmed gastritis characterized by dense infiltration of T lymphocytes onto the surface epithelium and pitted epithelium of the gastric mucosa, and the most common gastric mucosa. Lymphocytic gastritis can be complicated by pox-like gastritis, HP infection of gastritis , celiac disease, gastric mucosal folds, giant lymphadenopathy, lymphocytic colitis, collagenous colitis and other diseases, among which pox-like gastritis is the most common, the cause of this disease is unclear, may be a gastric mucosa to the disease mucosal tissue An immune response, the disease can also be independent of the disease.
2. Eosinophilic gastritis:
It is a chronic gastritis characterized by significant eosinophil infiltration in any layer or layers of the stomach wall. This disease occurs in patients with allergic or peripheral eosinophilia, or may be eosinophilic gastroenteritis. In part, the lesion is most likely to invade the antral mucosa. In children, the antrum involvement is almost 100%. Mucosal infiltration can cause erosion. When mucosal biopsy, eosinophils can be invaded into the epithelial cell layer, and epithelial cell necrosis can be seen. Regeneration, activated eosinophil degranulation, suggesting that tissue damage is caused by the release of toxic substances from eosinophils. Eosinophilic gastritis can also invade the antrum of the antrum, causing local stiffness, stenosis and emptying of the antrum.
