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Helicobacter pylori eradication may influence timing of endoscopic surveillance for gastric cancer in patients with gastric precancerous lesions: A retrospective study

Chronic atrophic gastritis and intestinal metaplasia related to Helicobacter pylori infection, are major risk factors for gastric adenocarcinoma. Eradication of H pylori and endoscopy surveillance of precancerous lesions may reduce the risk and/or lead to early detection of gastric cancer improving...

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Detalles Bibliográficos
Autores principales: Dore, Maria Pina, Cipolli, Alice, Ruggiu, Matteo Walter, Manca, Alessandra, Bassotti, Gabrio, Pes, Giovanni Mario
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5794400/
https://www.ncbi.nlm.nih.gov/pubmed/29369216
http://dx.doi.org/10.1097/MD.0000000000009734
Descripción
Sumario:Chronic atrophic gastritis and intestinal metaplasia related to Helicobacter pylori infection, are major risk factors for gastric adenocarcinoma. Eradication of H pylori and endoscopy surveillance of precancerous lesions may reduce the risk and/or lead to early detection of gastric cancer improving survival. In this study, the progression of precancerous lesions after H pylori treatment was evaluated. Patients with incomplete or complete intestinal metaplasia and/or gastric atrophy at the index endoscopy, were examined for the extension/histological worsening of precancerous lesions at the endoscopy surveillance for gastric cancer. Progression of lesions was evaluated according to H pylori status, age, and sex. Cox proportional hazard regression model and Kaplan–Meier curves were used to evaluate the strength of predictors for lesions progression. Among 105 patients (61 women) H pylori negative patients showed a milder worsening of gastric lesions between index and surveillance endoscopy compared with patients positive for the infection (log-rank test: P < .0001, P = .012, and P = .032 for antrum, angulus, and corpus, respectively). The Cox regression model showed persistence of H pylori infection (hazard ratio = 4.436; P < .0001) as the only relevant factor for lesion progression, whereas age >65 years and sex were not significant predictors. According to literature our results demonstrate that H pylori eradication is the major factor able to delay gastric precancerous lesions progression. Time interval for endoscopic surveillance in patients negative for H pylori infection and with gastric precancerous lesions may be extended.