Articles | Open Access | https://doi.org/10.55640/

ROLE OF H. PYLORI IN CHRONIC GASTRITIS AND ULCER DISEASE

Murtazayeva Khadicha Nuriddinovna, Eshkarayeva Muslima Pardayevna, Bakirova Marjona Bakirovna, Xolmirzayeva Xolisxon Zahriddinovna , Tashkent State Medical University

Abstract

 This article discusses in detail the crucial role of Helicobacter pylori infection in the etiology and pathogenesis of chronic gastritis and peptic ulcer disease. The adaptation of the microorganism to the acidic environment of the stomach (in particular, protection by the urease enzyme), the mechanisms of adhesion to epithelial cells, the release of cytotoxic factors and the activation of the local immune-inflammatory response are analyzed on a scientific basis. Also, the increased acid production as a result of increased gastrin secretion by the bacteria, the disruption of the protective barrier systems of the mucous membrane and, as a result, the formation of erosion and ulcer defects are explained step by step. The article reviews the morphological changes associated with H. pylori - lymphocytic and neutrophilic infiltration, glandular atrophy, intestinal metaplasia, destructive lesions of the mucous membrane - and their clinical manifestations in their interrelation. In addition, the practical importance of modern diagnostic methods (breath test, endoscopic biopsy, serological and fecal antigen tests) and the principles of eradication treatment are highlighted. The article substantiates the possibility of reducing the recurrence of chronic gastritis and ulcer disease and preventing complications through early detection and targeted treatment of H. pylori infection

Keywords

chronic gastritis, ulcer disease, Helicobacter pylori, inflammation, mucosa, acid secretion, eradication.

References

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World Health Organization. Guidelines for the management of Helicobacter pylori infection.

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ROLE OF H. PYLORI IN CHRONIC GASTRITIS AND ULCER DISEASE. (2026). International Journal of Medical Sciences, 6(4), 90-92. https://doi.org/10.55640/