What is the disposition of precancerous lesions?

What is “intestinal metaplasia”? “Intestinal epithelial metaplasia” is referred to as “intestinal metaplasia”, which refers to the development of chronic inflammation of the lower esophagus and chronic superficial gastritis into chronic atrophic gastritis, in which cells similar to intestinal mucosa appear in the epithelium of the esophagus and gastric mucosa, causing the secretion function of the normal esophagus and gastric mucosa to become absorption function. As the lower esophagus and gastric mucosa continuously absorb harmful substances or fail to remove them in time, some patients’ esophagus and gastric mucosa locally accumulate certain carcinogenic substances over time, and the long-term contact of carcinogenic substances with gastric mucosa finally leads to carcinogenesis. Precancerous lesions are not cancer. The so-called precancerous lesions only refer to the high possibility of esophageal and gastric cancer, not that they will definitely become cancerous in the future. Statistics show that the chance of cancer in barret esophagus is 10%, and the probability of cancer in “gastrointestinal metaplasia” is 5%. In other words, out of 100 patients with chronic gastritis and intestinal metaplasia, 5 patients may have bad changes. Therefore, it is important to overcome the “cancer fear” phenomenon. However, if intestinal metaplasia develops further into “atypical hyperplasia”, the probability increases to 25% or 40% (depending on the severity of the pathological changes). Therefore, in general, it is not necessary to be overly nervous about simple intestinal hyperplasia, and gastroscopy should be reviewed once a year. Strive for reversal through life conditioning and drug treatment. Maintain optimism, enhance confidence in treatment, develop good dietary hygiene habits, avoid taking drugs that are damaging to the gastric mucosa, etc. Food should be nutritious and light. Say goodbye to certain “convenience meals” and “foreign fast food” that are likely to produce carcinogenic substances during processing, do not eat Chinese hot pot that contains more spicy and stimulating condiments, and eat more vegetables and fruits and mixed grains. The diagnosis of intestinal epithelial hyperplasia in chronic gastritis is improving year by year with the popularity of endoscopy and medical advances. Due to the accelerated pace of life and increased work pressure, the number of patients suffering from atrophic gastritis with intestinal hyperplasia is also increasing year by year. Many professional books also refer to atrophic gastritis as “precancerous disease” and intestinal metaplasia of esophageal and gastric mucosa as “precancerous lesion”, so it brings a lot of mental burden to patients. At present, it is generally believed that gastric cancer develops from chronic superficial gastritis – atrophic gastritis – intestinal epithelial hyperplasia – atypical hyperplasia to gastric cancer. Intestinal epithelial hyperplasia of gastric mucosa, as an intermediate step in the multi-step hypothesis of gastric carcinogenesis, has been regarded as a precancerous lesion. However, not all intestinal epithelial metaplasia can be transformed into gastric cancer, and different subtypes have different prognosis. According to research data, complete intestinal chemosis has a low risk of gastric cancer, while colonic intestinal chemosis is strongly associated with the development of cancer. If atypical hyperplasia is found, it is a “precancerous lesion”. The number of patients with atrophic gastritis over the age of 40 has increased significantly, and in recent years it has been found that the incidence tends to be younger. It has been reported that 20% of adults have chronic atrophic gastritis. Chronic atrophic gastritis is often accompanied by pathological changes of intestinal epithelial metaplasia in some patients. This can manifest clinically as symptoms of dyspepsia, such as chronic, recurrent or persistent epigastric discomfort, early satiety, loss of appetite, nausea, vomiting, belching, loose and unformed stools. The occurrence of chronic gastritis is related to the following factors, such as H. pylori infection, long-term ingestion of coarse, irritating foods, overheated beverages, alcoholism, salty food, or food containing chemical irritants, taking non-steroidal anti-inflammatory drugs, poor lifestyle habits such as excessive smoking, long-term bile reflux, immune imbalance of the body, lack of nutritional factors, and genetic factors. Long-term adverse stimulation leads to damage to the gastric mucosal barrier, degeneration and necrosis of mucosal cells, and infiltration of a large number of inflammatory cells causing chronic gastritis. The stomach is an organ connected to the outside world and is constantly stimulated by the friction of food and swallowed bacteria and physical and chemical factors from three meals a day. It is very common for inflammation to occur in the gastric mucosa during a person’s lifetime, and if the mucosa of the entire stomach is examined, it is not uncommon for people to be found to have intestinal chemosis after the age of 40. The cancer risk of chronic gastritis is mainly for atrophic gastritis, but not all atrophic gastritis and intestinal metaplasia can become cancerous. How to treat intestinal hyperplasia? At present, there are more researches on intestinal metaplasia, but there is no specific medicine to treat it. Generally speaking, the treatment methods are as follows: (a) General treatment Try to remove the causative factors, such as maintaining an optimistic and open mood, enhancing confidence in treatment, developing good dietary and hygiene habits, avoiding foods and drinks that are irritating to the gastric mucosa, quitting smoking and alcohol, and avoiding drugs that are harmful to the gastric mucosa, such as non-steroidal anti-inflammatory drugs, etc. (2) Drug treatment 1. Helicobacter pylori eradication treatment Helicobacter pylori is one of the important causes of gastric mucosal lesions, and is also the “first killer” leading to the occurrence of gastric cancer. Studies have shown that H. pylori is involved in aggravating the destruction process of gastric mucosal epithelial cells, and H. pylori infection can lead to chronic gastritis and further promote gastric mucosal inflammation, so that gastric mucosal atrophy and enterosis gradually occur and progressively aggravate. Most studies have concluded that eradication of H. pylori infection can reduce, control or delay the aggravation of gastric mucosal atrophy and intestinal metaplasia, suggesting that eradication of H. pylori infection may reverse the intestinal epithelial metaplasia of gastric mucosa. 2, anti-bile reflux treatment Bile reflux can cause damage to the mucosa of the stomach and esophagus, leading to inflammation, ulcers, and even tumors. Therefore, it is of great concern. After bile reflux is corrected, it undergoes a long process of reversal, i.e. atypical hyperplasia – intestinal chemosis – atrophy – a continuous improvement process of chronic inflammation. As a long-term smoker and usually a fan of a couple of sips of wine, I recommend quitting smoking and drinking. Oral acid suppressants and antibiotics were administered, and regular follow-up reviews were conducted. As a result, the Barret’s esophagus and chronic gastritis were in remission when reviewed six months later.