Precancerous lesions of gastric cancer

Gastric precancerous lesions are first of all a histological concept, which refers to certain histopathological changes in the gastric mucosa. These lesions are more likely to become cancerous than normal or other gastric mucosal lesions, such as atypical hyperplasia of gastric mucosal epithelium and intestinal metaplasia of gastric mucosa. Whether it is gastric precancerous diseases or precancerous lesions, there are a few cases of canceration, but it does not mean that they will develop into cancer in the future. Most cases will have the possibility of stopping development or reversing after treatment. Gastric precancerous diseases are a clinical concept, which means that certain diseases have a higher chance of developing gastric cancer, such as gastric polyps, gastric ulcers, and chronic atrophic gastritis.

Gastric precancerous lesions are divided into two aspects: precancerous state and precancerous lesions. Gastric precancerous state refers to diseases before gastric cancer, such as CAG, ulcer disease, gastric polyps, residual gastritis and hypertrophic gastritis. These benign gastric diseases have a higher chance of developing gastric cancer. Among them, CAG is the most common gastric precancerous state.

The incidence of CAG is significantly increased in areas with a high incidence of gastric cancer. In the national epidemiological study of gastric cancer, the survey results of various areas with a high incidence of gastric cancer showed that there was a parallel relationship between the prevalence of CAG and the mortality rate of gastric cancer. Many scholars at home and abroad have conducted follow-up observations on CAG for varying periods of time, and the incidence of lesions is as high as 10%. The main pathological characteristics of CAG are chronic inflammation of the mucosa and glandular atrophy, often accompanied by gastric mucosal intestinal metaplasia (IM) and atypical hyperplasia. According to statistics, CAG is accompanied by intestinal metaplasia in 65.5%, and it increases with age. As the atrophic area expands, the proportion of intestinal metaplasia also increases.

Intestinal metaplasia cells come from proliferating cells in the neck of the glands proper. IM is divided into complete and incomplete types. The epithelium of complete intestinal metaplasia is well differentiated and is a common mucosal lesion with an inflammatory response. Incomplete colonic metaplasia, on the other hand, has poor epithelial differentiation and is highly detected in the mucosa adjacent to intestinal gastric cancer (88.2%), indicating that incomplete metaplasia is closely related to the occurrence of intestinal gastric cancer. Morson observed that 32.7% of 107 gastric cancers originated from intestinal metaplasia foci, Sugario found Panetb cells and goblet cells in early gastric cancer, and Tarri and other scholars observed that gastric cancer occurred in many intestinal metaplasia areas. Intestinal metaplastic cells may absorb certain lipids, which cannot be immediately transferred into the circulation due to the lack of lacteals, but are retained in intestinal metaplastic epithelial cells and become carcinogens. The pH and nitrite content in the gastric juice of CAG patients are significantly higher than those in normal gastric juice. The reason may be due to gastric gland atrophy, decreased gastric acid secretion, and increased nitrate reduction rate in the stomach, which reduces nitrate to nitrite, thereby increasing the synthesis of nitrosamine compounds in the stomach and causing cancer.

CAG is often accompanied by atypical hyperplasia of the gastric mucosa, which is a type of pathological histological change of the gastric mucosa that is prone to canceration. It is mainly characterized by excessive cell proliferation and loss of normal differentiation, and partial loss of similarity with the original tissue in structure and function, that is, atypia. Atypical hyperplasia of the gastric mucosal epithelium can occur in the gastric proper mucosal epithelium and glands, as well as in the epithelium and glands of intestinal metaplasia, so there is a distinction between gastric-type and intestinal-type atypical hyperplasia. Atypical hyperplasia can be divided into three levels: mild, moderate, and severe. According to clinical and pathological follow-up, mild and moderate atypical hyperplasia can be alleviated or return to normal, but severe atypical hyperplasia rarely returns to normal and can remain unchanged for many years or develop into gastric cancer.