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, 97 (4), e9734

Helicobacter Pylori Eradication May Influence Timing of Endoscopic Surveillance for Gastric Cancer in Patients With Gastric Precancerous Lesions: A Retrospective Study


Helicobacter Pylori Eradication May Influence Timing of Endoscopic Surveillance for Gastric Cancer in Patients With Gastric Precancerous Lesions: A Retrospective Study

Maria Pina Dore et al. Medicine (Baltimore).


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.

Conflict of interest statement

The authors declare that they have no competing interests.


Figure 1
Figure 1
In the upper panel; KM curves show the local worsening of lesions (from atrophy to metapalsia/displasia), subdivided according to H pylori status for each gastric segment (antrum, angulus, and corpus). Lower panel; KM curves expressing local extension of lesions (from antrum to angulus and from angulus to corpus) for patients subdivided by H pylori status. KM = Kaplan–Meier.

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