Abstract
Risk factors contributing to the transformation of chronic atrophic gastritis into gastric cancer are analyzed. Detection and monitoring of patients with precancerous conditions/lesions (precancerous changes), proper screening of H. pylori make early diagnosis of gastric cancer real. Features of precancerous conditions are given in order of increasing risk of developing gastric cancer. Adenomatous polyps of the stomach take the first place. Subsequent precancerous conditions include: cancer of the operated stomach, Menetria disease (hypertrophic gastropathy), B12-deficient anemia, and gastric ulcer. A definition of intestinal metaplasia subtypes is proposed as a risk factor for gastric cancer, dividing into complete and incomplete one, taking into account reduction in the expression of gastric mucins MUC1, MUC5AC and MUC6. Currently, the development of gastric cancer (mainly of the “intestinal type”) is considered as a multistage process involving the sequence of mucosal change, such as chronic inflammation, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma. Role of the organism’s genetic susceptibility to H. pylori infection, factors of pathogenicity contributing to epithelial metaplasia, are analyzed. Role of Toll-like type 4 receptors (TLR4) involved in the recognition of H. pylori is clarified. It is with this type of receptors that the development of an excessive immune response of the host is associated, resulting in damage to the mucous membrane in H. pylori-infected individuals. In particular, carriers of TLR4+896A> G polymorphism have a more severe atrophy of the stomach and degree of inflammation, as well as an increased risk of non-cardiac gastric cancer.
Highlights
Независимый диагноз Хронический гастрит (ХГ) не имеет большого прямого клинического значения
Features of precancerous conditions are given in order of increasing risk of developing gastric cancer
The development of gastric cancer is considered as a multistage process involving the sequence of mucosal change, such as chronic inflammation, atrophy, intestinal metaplasia, dysplasia and adenocarcinoma
Summary
В настоящее время развитие рака желудка (преи мущественно «кишечного типа») рассматривается как многостадийный процесс, включающий в себя по следовательность изменений СОЖ: хроническое вос паление, атрофия, кишечная метаплазия, дисплазия и аденокарцинома. В течение 30 лет у 50% инфицированных H. pylori развивается атрофия СОЖ, у 40% — кишечная метаплазия, у 8% — дисплазия, у 12% — аденокарцинома желудка. Pylori и воспаление СОЖ, что приводит к атрофии слизи стой оболочки и прогрессированию рака желудка. Meta-analysis: can Helicobacter pylori eradication treatment reduce the risk for gastric cancer? The long-term risk of gastric cancer after the successful eradication of Helicobacter pylori. В настоящее время развитие рака желудка (преимущественно «кишечного типа») рассматривается как многостадийный процесс, включающий в себя последовательность изменений слизистой оболочки: хроническое воспаление, атрофия, кишечная метаплазия, дисплазия и аденокарцинома. В частности, носители TLR4+896А>G полиморфизма имеют более тяжелую атрофию желудка и степень воспаления, а также повышенный риск некардиального рака желудка
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