Currently, Helicobacter pylori infection (H. pylori) is recognized as one of the most important risk factors for gastrocarcinogenesis. It is known that this infection does not directly cause neoplastic changes in the gastric mucosa, and this is due to a number of consecutive events due to the long persistence of the pathogen in the human body. The initial stage of this cascade, of course, is the inflammatory response, due to the body’s ability to adapt to extraneous infection, which is the inevitable result of the interaction of H. pylori with cells of the gastric epithelium. This direct damaging effect is enhanced by the production of vacuolating cytotoxin and the release of products of the cytotoxin-associated CagA gene, which, at a pathomorphological level, is manifested by inflammatory infiltration of the gastric mucosa (GM) to some extent. On the relationship between the degree of contamination and the activity of the inflammation of the GM in people infected with the CagA strain, today there are different, often conflicting opinions, which is why in this work we set the goal of establishing the relationship between the nature of the inflammatory response and the presence of the CagA gene in H. pylori- infected patients. The purpose of the study is to determinate the relationship between the nature of the inflammatory response and the genetic features of the H. pylori strain (CagA genotype).We examined 365 patients, among whom 40 people were included in the control group (18 women and 22 men, whose average age was 45,33±15,46 and 42,82±12,31, respectively) without any gastroenterological pathology in the anamnesis , patients with chronic non-atrophic gastritis (188 people) and chronic atrophic gastritis (137 people). A close relationship was established between the presence of the CagA gene, activity and the degree of contamination for chronic non-atrophic gastritis: for a low degree of contamination, Fisher’s exact test was = 0.002, p<0.05, for a moderate degree - 0.012, p<0.05, for a high degree - 0,012, p<0.05. Accordingly, in chronic atrophic gastritis: for a low degree of contamination Fisher’s exact test = 0.011, p<0.05, for a moderate degree - 0.003, p<0.05, for a high degree - 0.001, p<0.05. There is also a close relationship between the degree of contamination and the activity of chronic gastritis: in patients with a high degree of contamination, CG activity was determined, as a rule, for stage 2-3. In our study, the inflammatory response depended on the presence or absence of the H. pylori strain in the patient, which contains the CagA genotype, which, in our opinion, plays a key role in triggering a cascade of inflammatory changes in the GM and progression of chronic gastritis.

The precancerous potential of chronic gastritis (CG) associated with H. pylori is discussed in numerous writings, and today, CG is central to precancerous conditions of the stomach. A convincing theoretical basis for such an assessment of chronic gastritis is its characteristic feature — an interruption of cell renewal with the proliferation phase predominating over the differentiation phase. However, the determination of the degree of proliferative activity and impaired differentiation of the epithelium of the gastric mucosa (GM) remains not fully understood. The goal of our study was the immunohistochemical evaluation of the expression of Ki-67, Cyclin D1, p53, CPP32, HER2 and the Sox2 transcription factor in GM epithelial cells in patients with H. pylori-associated chronic gastritis.. To accomplish this goal, histological, cytological, immunohistochemical, molecular genetic, morphometric and statistical research methods were used. We found that in chronic H. pylori-associated non-atrophic gastritis (CNG) compared with H. pylori (-), the GM epithelium renewal rate increased, characterized by a significant increase in the expression of caspase-3 and Ki-67 proliferation markers, cyclin D1 (p <0.001) with expansion of the proliferative compartment and apoptosis zones. Ki-67, Cyclin D1, and p53 expression in severe dysplasia (SD) of GM was significantly (p <0.05) higher than the mild in patients with chronic non-atrophic and atrophic H. pylori-associated gastritis, despite a decrease in the expression of the transcription factor Sox2 and caspase-3 in cases of SD. The most specific marker for determining SD in patients with H. pylori-associated chronic gastritis was marker p53 (sensitivity 98.73%; specificity 83.38%, confidence interval 95%, p <0.05). Considering the immunohistochemical markers of H. pylori, a screening system has been developed for the early diagnosis of precancerous changes in the GM that will help optimize the treatment tactics of patients with chronic gastritis and increase the efficiency of detecting dysplastic and atrophic changes in the GM at their early stages of development.

Винницкий национальный медицинский университет им. Н.И. Пирогова г. Винница, Украина В статье приведены результаты обследования 27 пациентов в возрасте от 21 до 62 лет. Среди которых были 9 человек с хроническим атрофическим гастритом и полной кишечной метаплазией, 6 с ХАГ и неполной, 7 человек с умеренно дифференцированной аденокарциномой желудка и наличием кишечной метаплазии в близлежащих участках (5 мм от опухоли) и 5 человек с неизмененной СОЖ. Проводилось общеклиническое и фиброгастроскопическое исследование с прицельной биопсией и хромогастроскопией с использованием 10% ацетилцистеина и 1% раствора метиленового синего. Ключевые слова: кишечная метаплазия, слизистая оболочка желудка, лектины, патоморфологическая диагностика.