Aim. To assess the character of bacterial-viral infection of the gastric mucosa and dynamics of inflammatory process in adolescents with chronic gastritis in case of antihelicobacter therapy failure. Materials and methods. Seventy two adolescents with chronic gastritis aged 11–18 years (mean age 13.8 ± 0.4) were examined prior to and after antihelicobacter therapy. Results. It was established that after treatment against the background of regression of clinical symptoms, in most patients no positive dynamics of process manifestation or its progression was noted both in the body and antral part of the stomach. Conclusions. In the absolute majority of adolescents with the absence of Hp eradication (78.7 %) there was observed colonization with positive Hp strains and persistence of Epstein-Barr virus (68.1 %). It allows considering patients with such co-infection as a risk group for the absence of Hp eradication.

Objective. To establish the features of various clinical variants of chronic gastritis in childhood. Material and methods. 415 children aged 617 years with chronic Hp-associated gastritis were examined. The clinical and anamnestic data, the results of laboratory, endoscopic and morphological studies of gastrobioptates were analyzed. Genetic typing of Hp was carried out with the determination of 16 pathogenicity factors. The persistence of human herpes viruses of types 6 and 8 and Epstein Barr viruses in the gastric mucosa was determined. Results. The clinical heterogeneity of chronic gastritis in children with the allocation of four topical variants was established: isolated duodenitis, duodenogastritis, antrum gastritis, pangastritis. It was found that with the first two, a high frequency of giardiasis is registered, with antrumgastritis and especially pangastritis, a significant contamination of the gastric mucosa with Hp is detected, mainly of CagA and VacA-positive strains. It is proved that the persistence of the type 6 human herpes virus does not affect the severity of inflammation, while the presence of the Epstein-Barr virus increases it. Colonization of the gastric mucosa by highly pathogenic Hp strains significantly increases the severity and activity of inflammation. It is shown that atrophy of the gastric mucosa in children is uncertain, and true atrophic gastritis occurs only in 0.61 % of cases. Conclusions. Chronic gastritis in children is a heterogeneous pathology, and its individual variants differ significantly in etiological factors including infectious, pathogenetic mechanisms and features of the morphology of gastric mucosa. This should be taken into account when carrying out medical support for patients.

Objective. To evaluate the effect of the genetic characteristics of Helicobacter pylori on the nature of pathomorphological disorders in the gastric mucosa in chronic Hp-associated gastritis in young people. Material and methods. Forty-two adults (25 men and 17 women) aged 19 to 40 years with Hp-associated chronic gastritis were examined. The severity and activity of inflammation, as well as the presence of atrophy and intestinal metaplasia were determined in gastrobioptates. Genetic typing of Hp was performed for 16 pathogenicity factors of infect: CagA, CagM, CagT, CagH, CagC, CagF, CagE, VacAs1 and As2, IceA, Baba; HpaA; OipA, AlpB; UreB and UreI using polymerase chain reaction. Results. Pathogenic Hp strains were detected in 59.5 % of patients. Factors of adhesion HpaA (83.3 %), OipA (81 %), and AlpB (83.3 %) were identified with the highest frequency. In 57.1 % of cases, cytotoxin of the Cag group was detected, and 54.8 % of patients had a positive CagA-status. The VacA S1 allele was registered in 73.8 %, VacA S2 in 4.8 %, IceA in 38.1 %, and BabA in 45.2 % of cases. The presence of Hp strains in the gastric mucosa, which have three or more pathogenicity island genes, significantly increases the severity and activity of the inflammatory process, revealing signs of moderate atrophy of the digestive tract and intestinal metaplasia. Conclusions. Colonization of the gastric mucosa in young patients with Hp-associated chronic gastritis by highly pathogenic Hp strains leads to severe violations of its morphology.

Aim. To characterize the inflammatory process in gastric mucosa among adolescents with chronic gastritis in different variants of its bacterioviral infection. Materials and methods.Clinicoanamnestic, laboratory, endoscopic and morphological examination of 200 adolescents (age range 12–18 years) with chronic gastritis was carried out. In all patients, clinicoanamnestic data, standard laboratory study, esophagogastroduodenoscopy, gastrobiopsy followed by morphological analysis with visual analogue scale were assessed. According to the results of examination, all adolescents were divided into 4 groups depending on the character of bacterioviral infection of gastric mucosa. Results. No statistically significant differences were detected while comparing the rate of clinical manifestations of pain abdominal, dyspeptic, intoxication and asthenovegetative syndromes as well as changes, revealed in laboratory and ultrasound studies in the above mentioned groups of adolescents. Maximal presentation of macroscopic and pathohistological changes was registered in patients of group 4 (association between colonization of GM with highly pathogenic Hp strains and EBV persistence). Conclusions. The character of bacterioviral infection of gastric mucosa significantly determines the manifestation degree and activity of inflammatory process. The least degree of manifestation and activity of inflammatory process is registered when mucosa is colonized by low pathogenic Hp strains. Maximal presentation of macroscopic and pathohistological changes in the gastric mucosa is registered in adolescents with associated infection by high pathogenic Hp strains and Epstein-Barr virus. It is manifested by domination of marked and highly active inflammation and appearance of the signs of mucosal atrophy of gastric body and antrum.

The literature review highlights the questions of the interaction of Helicobacter pylori and the human body. Modern data on the structure of the pathogenicity island in the Helicobacter pylori genome are presented. There is given a detailed description of both well-known virulence and pathogenicity factors of the infection (genes encoding the formation of urease subunits, in particular urel, cytotoxin associated gene A, vacuolating cytotoxin gen A, blood group associated binding adhesion, induced by contact with epithelium) and less studied ones (sialic acid-binding adhesion, adhesion-associated lipoprotein A and B, adhesin gene of Helicobacter pylori, Hp outer membrane protein). The significance of individual genes and proteins encoded by them in the development of chronic inflammatory process in diseases of the upper digestive tract, as well as in ulcer and carcinogenesis is analyzed. Mechanisms of interaction of bacteria with epithelial cells of the gastric mucosa, adhesive and cytotoxic effects of Helicobacter pylori, factors of biofilm formation are described. The influence of the genetic structure of Infect on cytological composition of the gastric glands in the form of reduction of specialized glandular cells chief and parietal cells of pyloric glands and the increase of endocrine cells in the pool is assessed. It is shown that colonization of the gastric mucosa by highly pathogenic strains of Helicobacter pylori contributes to the development of widespread pronounced and active inflammation in it, the appearance of morphological signs of atrophy. The role of the genetic characteristics of the infection in the failure of anti-helicobacter therapy is emphasized. Separately, the question of the effect of combined infection of the gastric mucosa with highly pathogenic strains of Helicobacter pylori and Epstein-Barr virus is highlighted.