May 19, 2024

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Why does bile reflux get worse and develop into gastric cancer?

Why does bile reflux get worse and develop into gastric cancer?



Why does bile reflux get worse and develop into gastric cancer? Bile reflux gastritis has a certain relationship with the occurrence of gastric cancer. If bile reflux gastritis occurs, it needs active treatment, regular review and early treatment.



 What is bile reflux gastritis


Bile reflux gastritis refers to a pathophysiological phenomenon in which bile refluxes into the stomach. It is usually accompanied by the reflux of pancreatic juice into the stomach. This phenomenon also exists in normal people. Mild reflux can help reduce the acidity in the stomach. More reflux will damage the gastric mucosa.

Why does bile reflux get worse and develop into gastric cancer?

The mechanism of action is:


Bile acid can dissolve the mucus in the stomach and destroy the mucosal surface; bile can activate lecithinase a. Change lecithin into lysolecithin and destroy cell membranes. When the alkaline duodenal juice neutralizes the acidic gastric juice and the pH is close to neutral, pancreatin is activated, causing mucosal damage.


After partial gastrectomy and cholecystectomy, most patients have bile reflux.




Causes of bile reflux gastritis


1. Surgical sequelae

In some patients who have undergone gastrectomy and gastrojejunostomy, patients with pyloric dysfunction and chronic biliary diseases, bile can flow directly back into the stomach, and it is also easy to cause bile reflux gastritis.


2. Eating too fast or too full

Since the speed of gastrointestinal emptying is relatively fixed, when eating too fast or eating too much, food cannot enter the intestine smoothly, and bile reflux can also be induced.


3. Pylorus relaxation

Due to the relaxation of the pylorus, bile reflux gastritis is the mixing of bile in the duodenum with other intestinal juices, passing through the pylorus, flowing backwards into the stomach, stimulating the inflammation of the gastric mucosa, and after the occurrence of lesions, bile reflux is formed. gastritis.


4. Irregular diet

Since the gastrointestinal tract has its own physiological frequency (biological clock), it is generally advocated that it should be relatively stable relative to the meal time. If the regular diet is irregular, it will cause the gastrointestinal to “rest” after eating and the relative lack of motivation will cause reflux.


5. The mechanism of duodenal gastrointestinal reflux

Duodenal gastrointestinal reflux is a physiological phenomenon of the body, but if it occurs excessively, it will cause damage to the gastric mucosa. When reverse peristalsis of the duodenum occurs, and the pylorus is opened at this time, duodenal gastrointestinal reflux occurs. Sometimes the reverse peristalsis of the duodenum is very strong, if there is a strong antral contraction. It can also prevent the occurrence of duodenal gastrointestinal reflux. Any factor that causes gastrointestinal motility disorder and anatomical abnormality can cause pathological duodenal gastrointestinal reflux.


6. Pathogenic effects of duodenal gastrointestinal reflux

Bile acid is the main component of the mucosal damage caused by duodenal reflux fluid, which has a significant damaging effect on the mucosal barrier. In an acidic environment, the invasiveness of juice acid on the gastric mucosa is enhanced, and its combined action with digestive enzymes and other components can cause changes in mucosal cells and tissue structure, weaken the various protective mechanisms of the gastric mucosa, and promote the action of other damage factors such as gastric acid And the role of Helicobacter pylori.


7. Helicobacter pylori infection

Helicobacter pylori infection causes gastric mucosal inflammation. Bile reflux gastritis can coexist with HP infection. Both HP infection and bile reflux are related to mucosal damage, which may affect the gastroduodenum by increasing the release of gastrin Motivation, causing bile reflux.


8. Other reasons

For example, primary pyloric sphincter dysfunction can prolong the open time of the pylorus, relax the pylorus or keep it open, causing the contents of the duodenum to flow back into the stomach, causing duodenal gastrointestinal reflux; such as gastrointestinal neuropeptides and Abnormal levels of hormones can cause disturbances in gastrointestinal motility and lead to duodenogastric reflux.




What are the symptoms of bile reflux gastritis?


The main clinical symptoms of bile reflux gastritis are as follows:


  1. Pain in the upper abdomen and vomiting of bile. The nature of the pain in the upper and middle abdomen is burning pain, which is aggravated after eating, and is often accompanied by nausea, vomiting, and spitting out a pale yellow bile mixture. Often mixed with food. Some also have symptoms such as melena, hematemesis, weight loss and so on.
  2. After fasting, the pain in the upper abdomen can increase.
  3. The effect of taking antacids is poor.
  4. Anemia often occurs.


A small number of patients may present as pain behind the sternum, or a feeling of indigestion in the stomach. Bile vomiting is its characteristic performance. Due to gastric emptying disorder, vomiting usually occurs in the evening or midnight. The vomit may be accompanied by food and occasionally a small amount of blood. Because of fear of worsening symptoms after eating, patients reduce their food intake, which can lead to symptoms such as anemia, weight loss, malnutrition, and diarrhea.



 What are the effects of bile reflux on human health?


It is currently believed that bile reflux can cause inflammation, ulcers and tumors in the upper gastrointestinal tract, which means that long-term bile reflux can lead to esophagitis, gastric mucosal erosion, hyperplasia, active inflammation, gastric ulcers, and even gastric cancer. It is importantly related to the occurrence of upper gastrointestinal inflammation, ulcers, and tumors.



Bile reflux may cause cancer!


The possible carcinogenic mechanisms of bile reflux are as follows:


1. The direct damage effect of bile on gastric mucosa.


We know that bile is produced by the liver, and its main function is to help digestion and absorption. The main part of the effect is in the intestine. Under normal circumstances, cholesterol in the liver synthesizes primary bile acids, and after entering the intestinal cavity, secondary bile acids are formed under the action of bacteria. The toxicity of secondary bile acids is stronger than that of primary bile acids. Lithocholic acid is the most toxic.


During bile reflux, secondary bile acids and free bile acids flow back into the stomach, which can destroy the lipoprotein layer of gastric epithelial cells, thereby destroying the gastric mucosal barrier.


The pancreatic juice in the reflux also has a damaging effect on the gastric mucosa. Phospholipase A in the pancreatic juice and lecithin in the bile are converted into lysolecithin, which can remove mucus and damage the gastric mucosal barrier by dissolving the phospholipids in the epithelial cell membrane of the gastric mucosa. The hydrogen ions diffuse into the gastric mucosa due to the damage of the barrier mechanism, thereby activating pepsinogen, increasing the permeability of the mucosa and causing gastric mucosal damage.


2. Bile reflux provides conditions for other factors to damage the gastric mucosa.


Bile reflux directly affects the chemical environment in the gastric cavity and on the surface of the mucosa, enhancing the pathogenic effects of gastric acid and Helicobacter pylori harmful factors, and aggravating the pathogenic effects of the above factors.


Studies believe that after bile flows back into the stomach, soluble bile acids enter mucosal cells in a non-ionized lipophilic state, and can accumulate up to 8 times the luminal concentration, causing damage to the cell membrane and its tight junctions.


Therefore, the reflux of duodenal contents such as bile participates in chronic gastric mucosal injury.


3. Bile reflux after gastrectomy can destroy the mucosal barrier of the remnant stomach.


The occurrence of residual gastritis in patients with gastric antrum resection is also related to decreased gastrin secretion, gastric mucosal atrophy, changes in blood flow, and changes in mucosal surface properties after gastric antrum resection. Therefore, the gastric mucosal barrier is more susceptible to bile damage, which is conducive to H+ reaction. Diffuse and damage the gastric mucosa.


The destruction of gastric mucosal barrier by bile acids and bile salts is also one of the most important mechanisms for the occurrence of gastric ulcer. Studies believe that the damage of bile reflux to gastric mucosa is mainly manifested as active inflammation, intestinal metaplasia, gland atrophy and localized hyperplasia, while chronic atrophic gastritis, gastric mucosal dysplasia or intestinal epithelial metaplasia, gastric glands Cystic dilation, etc. are considered to be pre-cancerous lesions of the stomach.


4. Bile reflux leads to an increased risk of gastric cancer.


The remnant stomach after distal gastric surgery is now considered a precancerous lesion of gastric cancer. The mechanism of remnant gastric cancer may be related to the following factors:


(1) After partial gastrectomy, the normal physiological anatomical relationship of the gastrointestinal tract is changed, leading to major pathophysiological changes in the gastric mucosa, which is an important pathological basis for the occurrence of remnant gastric cancer. Mainly after partial gastrectomy, the normal pyloric function is lost, and a large amount of bile and pancreatic juice flows back into the remnant stomach, causing strong stimulation and damage to the gastric mucosa.


(2) After gastrectomy, the mucosal barrier function of the remnant stomach is damaged. Due to the removal of the pylorus and gastric antrum, the lack of G cells to secrete gastrin, gastric mucus secretion decreases, glands atrophy, and the remnant stomach is in a low or acid-free state, so alkaline reflux fluids such as bile are more likely to damage the gastric mucosa, especially It is the defatted lecithin in the bile that has a strong damaging effect on the gastric mucosal barrier mechanism.


(3) Bile reflux leads to long-term low acidity in the stomach, which is conducive to bacterial reproduction, especially the increase of bacteria with nitrate reductase and the increase of carcinogens-nitrosamines, which may also increase the chance of remnant gastric cancer.


It can be seen that there is a certain relationship between bile reflux gastritis and the occurrence of gastric cancer. If bile reflux gastritis occurs, it needs active treatment, regular review and early treatment.


(source:internet, reference only)

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Important Note: The information provided is for informational purposes only and should not be considered as medical advice.