Gastric cancer prevention – screening means is the key Regardless of the presence of lymph node metastasis, the cancerous tissue in early gastric cancer is only confined to the gastric mucosal layer or submucosal layer. Early gastric cancer has two special types, among which microgastric cancer
cancer is early gastric cancer with the maximum diameter of lesion ≤5 mm, while small gastric cancer is early gastric cancer with the maximum diameter of lesion >5-10 mm.
The precancerous condition of the stomach includes precancerous diseases (discases) and pre-cancerous diseases.
discases) and precancerous lesions.
lesions). The former refers to benign gastric diseases associated with gastric cancer, which have the risk of gastric cancer and are clinical concepts, such as chronic atrophic gastritis, gastric ulcer, gastric polyp, postoperative gastric, Menetrier’s disease (hypertrophic gastritis), etc. The latter refers to pathological changes that have been proven to be closely related to gastric carcinogenesis, i.e., heterogeneous hyperplasia or intraepithelial
neoplasia), which is a pathological concept. Intraepithelial neoplasia is a precancerous lesion characterized by morphological abnormalities in cytology and structure, genetic clonal alterations in genetics, and biological behavior that predisposes to progression to invasive and metastatic invasive carcinoma. Intraepithelial neoplasia is divided into two grades, namely low-grade intraepithelial neoplasia (low-grade intraepithelial neoplasia) and low-grade intraepithelial neoplasia (low-grade intraepithelial neoplasia).
intraepithelial intraepithelial neoplasia (LGIN) and high-grade intraepithelial neoplasia (high-grade).
LGIN corresponds to mild and moderate heterogeneous hyperplasia, and HGIN corresponds to severe heterogeneous hyperplasia and carcinoma in situ. As we all know, gastric carcinogenesis is divided into five parts, and different states have different treatment options. According to the 1998 Vienna pathological staging criteria for gastrointestinal epithelial tumors, see the table below, different clinical management is selected according to different endoscopic and pathological diagnoses. If we control the disease in any state before early gastric cancer and intervene and review it regularly, we can well prevent the occurrence of gastric cancer. And most of our gastric cancer patients are already in the middle and late stage when they are diagnosed, so early diagnosis and early treatment are especially important for patients’ prognosis. Currently, gastroscopy combined with gastric mucosal biopsy is the gold standard for diagnosing gastric cancer, but the test is invasive and not suitable for screening and census. Therefore, there is an urgent need for a simple, rapid, reproducible, non-invasive and dynamic monitoring test as a screening method for gastric cancer, as well as for diagnosis and monitoring of lesion development at the stage of atrophic gastritis. Gastric function test is a method to determine gastrin 17 (G-17) and pepsinogen I and II (PG I and II) by taking 2-3ml of venous blood (fasting) and analyzing them to assist in the diagnosis of gastric mucosal diseases. G-17 is a non-invasive, painless, safe and economical method to detect gastric diseases. Serum gastrin is a gastrointestinal hormone secreted mainly by G cells in the gastric sinus and duodenum, which plays an important role in regulating the function of the digestive tract. More than 95% of biologically active gastrin in the human body is α-amidated gastrin, of which 80%-90% is G-17 and 5%-10% is G-34. In atrophic gastritis, where sinus atrophy is the main cause, sinus mucosal atrophy can lead to a decrease in the number of G cells and a decrease in G-17 secretion, resulting in a lower G-17 level in the blood circulation, so serum G-17 level can be used as a gastric sinus Therefore, serum G-17 levels can be used as a serum marker for atrophic gastritis, and studies have shown that the optimal threshold value of G-17 for the diagnosis of atrophic gastritis is 5.1
G-17 was negatively correlated with the severity of gastric sinus atrophy. PG
PG (pepsinogen) is an aspartate protease precursor secreted by the gastric mucosa, mainly divided into PGⅠ and PGⅡ, PGⅠ is mainly secreted by the main cells and the mucus neck cells of the fundic glands; PGⅡ is secreted by the main cells, but also by the mucus neck cells of the urinary glands, the mucus cells of the cardia and pylorus glands, and the Brunner’s gland of the upper duodenum.
PG is not only helpful to determine whether the gastric mucosa is atrophied, but also to identify the site and severity of atrophy. Studies have shown that PG I and PG II levels are positively correlated with the activity and extent of chronic inflammation in the gastric sinus and body, and PGR (PG
I/ PG II) was negatively correlated with the latter two. The following graphs show the relationship between pepsinogen and gastric disease. The 2014 Consensus Opinion on Early Gastric Cancer Screening and Endoscopic Diagnosis and Treatment in China states that a decrease in PG I concentration and/or PGR is suggestive of atrophic gastritis, and usually PG I ≤ 70 μg /L
and PGR≤3.0 as the threshold value for the diagnosis of atrophic gastritis, and serum PGⅠ≤70 μg/L and PGR≤7.0 were used for gastric cancer screening in high prevalence areas in China.
Studies have shown that low serum PG I levels and PGR are biological markers of gastric atrophy, and serum PG I levels gradually decrease with increasing severity of mucosal atrophy, with PGR being particularly significant. Therefore, in order to further reduce the underdiagnosis rate of early gastric cancer, the clinical diagnosis of early gastric cancer can be based on “ABC method plus endoscopy”, and if there are three obvious abnormalities in gastric function, further fine endoscopic examination can be performed, including narrow band imaging (NBI), intelligent electronic spectroscopy (FICE), intelligent electronic staining endoscopy (I-SCAN). (I-SCAN), which can not only reduce patient pain and waste of medical resources, but also improve the diagnosis rate of early gastric cancer.