PATHOPHYSIOLOGY OF GASTRITIS AND CORRELATION WITH H. PYLORI: AN IN-DEPTH INVESTIGATION AND ITS CLINICAL IMPLICATIONS
Keywords:
Gastritis, Pathophysiology, Helicobacter pyloriAbstract
Gastritis is an inflammation of the gastric mucosa that can be triggered by several factors, such as prolonged use of some medications, smoking, and infection by the bacterium Helicobacter pylori (HP). The prevalence of this infection encompasses approximately half of the world population, and although its relationship with gastritis has not been fully elucidated, it is known that bacterial virulence, the host's immune system, and environmental influences interact to constitute a complex mechanism that establishes different gastritis phenotypes. These different phenotypes can be distinguished in chronicity, severity, late diagnosis, response or refractoriness to treatment, and clinical complications. This literature review aims to explore the pathophysiology of Helicobacter pylori-associated gastritis and its clinical implications, in order to provide a comprehensive understanding of this condition and its implications for medical practice, addressing its association with peptic ulcers, gastric cancer, and anemia, as well as reviewing available therapeutic options against this infection. To this end, 154 articles were identified, and of these, 18 were selected for this study based on the inclusion and exclusion criteria adopted. Thus, the potentiating action of H. pylori in the development of some gastroenterological diseases was observed, as seen in the increase in the genetic expression of PREX2, found in cancer cells, and in the endoscopic findings of antral nodularity, both due to this bacterium, which allows us to conclude the close relationship of gastritis with clinical implications of intense severity and in the long term.
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Copyright (c) 2024 Ana Carolinne Guerreiro Duarte, Bruna Wu Zhao, Clarissa de Deus Lemos, Kézia Signer Santos, Lanna Samara de Carvalho Araújo, Millena Lima Pascoal Moura, Yasmin de Deus Lemos, Patricia Alves Silva

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