Affiliation:
1. Research Institute for Medical Problems in the North-Division
2. Krasnoyarsk State Medical University named after Professor V.F. Voino-Yasenetsky;
Krasnoyarsk Regional Skin and Venereological Dispensary No. 1
Abstract
Introduction. It is known that the presence of the CagA gene in Helicobacter pylori is associated with its increased pathogenicity. However, in children, studies on the effects of this strain on the gastric mucosa are insufficient.Aim. To compare effects of different Helicobacter pylori (HP) strains on the gastric and duodenum mucosa in children to optimize indications for eradication.Materials and methods. 397 adolescents (169 boys and 227 girls) aged 11–18 were examined on the basis of the hospital gastroenterological department: the content of antibodies to the CagA strain of HP was determined by ELISA, esophagogastroduodenoscopy (EFGDS) was performedwith a biopsy of the gastric mucosa and determination of the HP contamination degree, and also HP gene was detected in the feces.According to the results obtained, all children were divided into 3 groups: 131 children (57 boys and 74 girls) infected with CagA by negative HP strains (CagA “-”); 119 children (52 boys and 67 girls) infected with CagA positive HP strains (CagA “+”); 94 children (36 boys and 57 girls) who are not infected with HP (HP “-”).Results. When we analyzed the endoscopic-histological picture of the gastric mucosa in the CagA “+” group, in contrast to the CagA “-” group, it was found that the chances of developing highbacteria contamination of the mucosa increased 4.7 times, II and III degree of gastritis activity – 6.6 times, chronic inflammation – 2.6 times, hyperplastic gastritis – 2.8 times, erosive gastritis or duodenitis – 2.7 times, peptic ulcer – 3.6 times, andalso signs of concomitant candidiasis (the presence of structural elements of the Candida fungus) – 4.1 times.Conclusion. Thus, it is advisable for all children with gastroduodenal pathology to recommend an examination for the detection of the CagA HP antigen with subsequent eradication.
Reference14 articles.
1. Pimanov SI, Makarenko EV. Optimized eradication protocols: recommendations of the American gastroenterologist board, Masstrikht v/Florentine and Toronto consensuses. Meditsinskiy Sovet. 2017;(15):10–17. (In Russ.) https://doi.org/10.21518/2079-701X-2017-15-10-17.
2. Stepanov YuM., Budzak IYa. Maastricht Consensus 5: An analytical overview of the provisions. Gastroenterology. 2017;(1):36–45. (In Russ.) https://doi.org/10.22141/2308-2097.51.1.2017.97870.
3. Shurgina IS, Gulyaev AN. Helicobacter pylori infection: a modern look at the problem. Vestnik of Saint Petersburg University. 2007;(1):29–38. (In Russ.) Available at: https://www.elibrary.ru/rtsimf.
4. Higashi H, Tsutsumi R, Muto S, Sugiyama ST, Azuma T, Asaka M, Hatakeyama M. SHP-2 tirosine phosphatase as an intracellular target of Helicobacter pylori CagA protein. Sciense. 2002;295(5555):683–686. https://doi.org/10.1126/science.1067147.
5. Ageeva ES. Еffects of cytokines in pathogenesis of Нelicobacter pyloriassociated chronic gastritis and ulcer disease. Siberian Medical Journal (Irkutsk). 2014;(2):5–8. (In Russ.) Available at: https://www.elibrary.ru/sfpjrf