Chronic Atrophic Gastritis: Risk Factors and Patient Screening (Literature Review)

The review highlights the main aspects of screening for early gastric cancer (EGC), including the collection of an anamnesis and the use of the combined serum antibody determination of IgG class to H. pylori and pepsinogen (PGI, PGI / PGII) by ABC for screening of chronic atrophic gastritis (CAG) and EGC. Non-invasive screening in the population is used to identify patients at high risk for developing CAG and EGC for further endoscopic and morphological studies. According to the results of non-invasive screening, patients are identified in groups A, B, C, D. Group A does not need further endoscopic and morphological examination. In groups B, C, D, these examinations are conducted every 1, 3, 2 years and annually, respectively. The role of H. pylori as a carcinogen of the first order is emphasized, however eradication is most effective before the development of pronounced irreversible changes in the gastric mucosa. Anti-Helicobacter therapy largely reduces atrophy in the mucous membrane of the body of the stomach, to a certain extent reducing chronic inflammation. The impact on all mechanisms of the inflammatory process in the mucosa is an important strategic task in reducing the progression of atrophic changes in the mucosa. It is noted that eradication of H. pylori is most effective in slowing the progression of carcinogenesis, if performed prior to the development of the stage of H. pylori-associated atrophic gastritis and / or dysplasia. For the management of patients with CAG, two integral indicators are important according to the results of endoscopic examination with a biopsy of gastric mucosa: 1) the severity of the inflammatory process (infiltration with neutrophils and mononuclear cells); 2) the severity of atrophy - the so-called Operative Link for Gastritis Assessment (OLGA-2008). This system makes it possible to determine the stage of atrophy with stratification of the risk of gastric cancer (GS). After treatment, it is important to determine the degree of regression of inflammation and atrophy. In stage I atrophy of the gastric mucosa, the risk of developing gastric cancer is minimal, in stage II it is moderate, and in stage III and IV atrophy it is high. It can be reduced more effectively if the eradication of H. pylori is carried out before precancerous gastric mucosa measurements with minimal risk on the OLGA system. Conclusion. Combined use of non-invasive and invasive methods in the detection of chronic atrophic gastritis and EGC allows to identify in the population of the high-risk group and to carry out purposefully endoscopic and morphological research. The strategy of using these methods allows for effective prevention and detection of chronic atrophic gastritis, dysplasia, and early gastric cancer.