Intestinal metaplasia is a precancerous lesion of gastric cancer. Epithelial cells of stomach and esophagus are changed or replaced by goblet cells. Goblet cells are large round hollow cells, which are usually found in the intestine; They should not appear in the stomach or esophagus. The function of goblet cells is to preserve and protect the mucus layer of the intestine by producing and secreting a thick mucus layer.
Although intestinal metaplasia is defined by intestinal differentiation, it is heterogeneous in molecule, but it can be divided into complete or incomplete subtypes in histology. Complete intestinal metaplasia (type I) is similar to small intestinal epithelium, with goblet cells, Paneth cell, eosinophilic intestinal cells and brush border. It is related to the deletion of gastric mucin markers (MUC 1, MUC5AC, MUC6) and the expression of mucin MUC2 in intestinal saliva. Incomplete intestinal metaplasia is more similar to large intestine epithelium, lacking absorptive cells, but with columnar cells similar to gastric vesicle cells. It has no brush border and usually maintains the expression of gastric mucin markers (MUC 1, MUC5AC, MUC6) together with MUC2. Incomplete intestinal metaplasia is further subdivided into type ⅱ intestinal metaplasia, in which cells express a mixture of neutral mucin and intestinal sialoprotein, and their cells express sulfadiazine. In practice, the histopathological classification between complete and incomplete intestinal metaplasia is usually not mutually exclusive, and tissue fragments contain two subtypes of components. Complete and incomplete intestinal metaplasia is very important in clinic, because incomplete intestinal metaplasia seems to develop into cancer more easily.
Intestinal metaplasia may develop into adaptive and protective lesions under the condition of long-term infection of Helicobacter pylori. At present, a lot of work has been done to determine how Helicobacter pylori infection leads to intestinal metaplasia, which involves many genes, including SOX2 and CDX2. SOX2 is a transcription factor involved in gastric differentiation and negatively regulates intestinal differentiation, while CDX2 is a key intestinal transcription factor involved in establishing and maintaining intestinal metaplasia. SOX2 and CDX2 seem to be under the reverse regulation of Helicobacter pylori. Complete intestinal metaplasia was SOX2 negative (93%), and incomplete intestinal metaplasia was mainly SOX2 positive (85%). In addition, it has been proved that the expression of CDX2 is partly induced by NF-κB-dependent mechanism after Helicobacter pylori infection.
Gastroduodenal reflux is another proposed gastritis, which can cause chronic gastritis and intestinal metaplasia, similar to gastroesophageal acid reflux in Barrett's esophagus. A large-scale study involving 2283 patients reported that the incidence of intestinal metaplasia increased after exposure to bile acids. In this case, the occurrence of intestinal metaplasia may represent a protective mechanism, that is, intestinal metaplasia is more resistant to bile than normal gastric mucosa.
Symptoms of intestinal metaplasia
Most people have no obvious symptoms of intestinal metaplasia. Others may have symptoms of stomach upset, such as gastric acid reflux, gastroduodenal ulcer, gastritis or gastroesophageal reflux disease (GERD), but these symptoms may be caused by other root causes.
cause
Although the exact cause of intestinal metaplasia has not been confirmed, it is generally believed that Helicobacter pylori infection is the main potential culprit.
What is Helicobacter pylori?
According to the Journal of Gastroenterology, more than 50% people in the world may be infected with Helicobacter pylori. Helicobacter pylori is a bacterium that infects the stomach. It usually occurs in childhood and is a common cause of gastroduodenal ulcer. In fact, a study on patients with Helicobacter pylori in Africa in 20 19 found that about 90% to 100% of duodenal ulcers were caused by Helicobacter pylori, while 70% to 80% of peptic ulcers were caused by Helicobacter pylori infection. This study also found that 38.6% of intestinal metaplasia was also diagnosed as Helicobacter pylori infection.
As we all know, Helicobacter pylori will invade the stomach wall. This is also one of the reasons why many experts believe that infection is directly related to the development of intestinal metaplasia. Another study in China involved 1600 healthy participants (average age 42 years) infected with Helicobacter pylori, and found that their intestinal metaplasia rate was 29.3%.
The median time for intestinal metaplasia to progress to gastric cancer is estimated to be 6. 1 year, while mild dysplasia is only 2.6 years.
Risk factor
Intestinal metaplasia is very common in the world. For diagnostic purposes, one in four people who undergo gastroscopy has intestinal metaplasia. Specific factors that increase the risk of intestinal metaplasia are found to include:
The existence of helicobacter pylori infection
There are patients with gastric cancer among the first-degree relatives.
Lack of vitamin c in diet
smoke
Age (risk increases with age)
Intestinal metaplasia is a precancerous state. Without treatment, abnormal cells in the stomach will go through a stage called dysplasia. Atypical hyperplasia is the existence of abnormal cells in tissues, which may constitute a stage before cell canceration. The reduction of risk factors may reduce the possibility of intestinal metaplasia and the chance of these cells developing from atypical hyperplasia to cancer cell stage. Risk factors include:
Genetic factors: when a person has a family history of gastric cancer or other intestinal diseases, he may be more prone to the risk of intestinal metaplasia of gastric cancer.
alcohol
Long-term acid reflux
Secondhand smoke (and other toxins in the environment)
? Smoking: This lifestyle factor may increase the risk of many health-related diseases, including the risk of intestinal metaplasia called Barrett's esophagus. Smoking will increase the incidence of gastric cancer in the upper stomach near the esophagus; The chances of smokers suffering from gastric cancer have doubled.
diagnose
In many cases, intestinal metaplasia is found when medical staff check other digestive system problems (except intestinal metaplasia). Because intestinal metaplasia is probably asymptomatic (asymptomatic), gastroscopy and histological examination are needed to confirm the diagnosis.
Endoscopic examination results of intestinal metaplasia. A) White light endoscopic images showed intestinal metaplasia with pale white spots. B) Narrow-band imaging enhances the contrast of mucosa and highlights intestinal metaplasia plaques. C) Magnified endoscopy revealed a light blue peak (LBC) on the epithelial surface; In some cases, white opaque substance (WOS) can be seen in the middle part of the concave opening. D) corresponds to the white square in image c.
prevent
According to a study in the World Journal of Gastrointestinal Oncology, gastric cancer is the second most common cause of cancer-related death in the world. The paper also pointed out that intestinal metaplasia is a precancerous lesion, which can increase the risk of gastric cancer by 6 times. Therefore, screening and preventive measures are very important. Follow-up measures to prevent precancerous lesions can ensure that cancer cells have not started to grow and diagnose the growth of cancer cells as soon as possible, which is a key preventive measure.
So far, there is not enough clinical research to clearly prove that changing lifestyle can effectively treat intestinal metaplasia. However, preventive treatment can be prescribed, including changing diet to lower gastric acid levels. Diet is considered to help prevent intestinal metaplasia from becoming gastric cancer, because diseases such as chronic (long-term) gastric acid reflux and GERD (involving hyperacidity) may increase the risk of cell abnormalities and cancer.
Dietary changes are considered to reduce the risk factors of intestinal metaplasia (and may help reduce the growth of Helicobacter pylori), including;
Light diet (non-spicy diet, low in fat and oil)
High-fiber, whole-food diet (rich in fresh fruits and vegetables, excluding processed sugary and high-fat foods)
Whole grain diet (food made instead of white flour)
treat cordially
A research report of 20 19 said: "Finding a way to eliminate Helicobacter pylori bacteria may help reduce the risk of intestinal metaplasia.
If the patients with intestinal metaplasia are positive for Helicobacter pylori infection, antibiotics can be selected to eliminate Helicobacter pylori. Antibiotic treatment usually lasts about 14 days. Another treatment that can be provided for intestinal metaplasia may include drugs that reduce acid in the stomach and esophagus to reduce tissue inflammation.
It should be noted that Helicobacter pylori is a common bacterium that grows in the digestive tract. Therefore, one of the keys to prevent intestinal metaplasia is to check Helicobacter pylori regularly. Healthy diet, rich diet, full-fat food, low saturated fat and unhealthy sugar are another measure to reduce the risk of intestinal metaplasia.