4.7 Article

Reversibility of atrophic gastritis and intestinal metaplasia after Helicobacter pylori eradication - a prospective study for up to 10 years

Journal

ALIMENTARY PHARMACOLOGY & THERAPEUTICS
Volume 47, Issue 3, Pages 380-390

Publisher

WILEY
DOI: 10.1111/apt.14424

Keywords

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Funding

  1. National Research Foundation (NRF)
  2. Ministry of Science, ICT and Future Planning (MSIO)

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Background: Atrophic gastritis and intestinal metaplasia are premalignant conditions for gastric cancer. Their reversibility by Helicobacter pylori eradication remains controversial. Aim: To evaluate the reversibility of atrophic gastritis and intestinal metaplasia by H. pylori eradication with long-term follow-up. Methods: 598 subjects were prospectively enrolled and followed for up to 10 years. They were categorised as H. pylori-negative (n = 65), H. pylori non-eradicated (n = 91), and H. pylori-eradicated (n = 442). Histological assessment was performed for antrum and corpus by Sydney classification. Results: Histological follow-up was performed regularly at 1, 2, 3-4 and 5 years, with mean follow-up of 1.07 0.21, 2.29 +/- 0.83, 3.93 +/- 1.02, and 6.45 +/- 1.28 years, respectively. Atrophic gastritis in antrum and corpus gradually and significantly (both P < .05 for all timepoints) improved only in the H. pylori-eradicated group compared to that at baseline. Significant difference in atrophic gastritis between H. pylori-eradicated and H. pylori-negative groups disappeared from 1-year follow-up. Similarly, intestinal metaplasia in antrum and corpus improved significantly (both P < .05 for all timepoints) only in the H. pylori-eradicated group in comparison with that at baseline. Significant difference in intestinal metaplasia between H. pylori-eradicated and H. pylori-negative groups disappeared from 5 years of follow-up in the antrum and from 3 years of follow-up in the corpus. Conclusion: H. pylori eradication may be a preventative strategy for intestinal-type gastric cancer by regression of atrophic gastritis and intestinal metaplasia.

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