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Helicobacter pylori eradication treatment and the risk of gastric adenocarcinoma in a Western population
  1. Eva Doorakkers1,
  2. Jesper Lagergren1,2,
  3. Lars Engstrand3,4,
  4. Nele Brusselaers3,4
  1. 1 Upper Gastrointestinal Surgery, Department of Molecular Medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden
  2. 2 School of Cancer Sciences, King’s College London, London, UK
  3. 3 Centre for Translational Microbiome Research, Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden
  4. 4 Science for Life Laboratory, Stockholm, Sweden
  1. Correspondence to Dr Eva Doorakkers, Upper Gastrointestinal Surgery, Department of Molecular medicine and Surgery, Karolinska Institutet, Karolinska University Hospital, Stockholm 17176, Sweden; eva.doorakkers{at}ki.se

Abstract

Objective Gastric infection with Helicobacter pylori is a strong risk factor for non-cardia gastric adenocarcinoma. The aim of this study was to assess whether the risk of gastric adenocarcinoma and non-cardia gastric adenocarcinoma decreases after eradication treatment for H. pylori in a Western population.

Design This was a nationwide, population-based cohort study in Sweden in 2005–2012. Data from the Swedish Prescribed Drug Registry provided information on H. pylori eradication treatment, whereas information concerning newly developed gastric adenocarcinoma was retrieved from the Swedish Cancer Registry. The risk of gastric adenocarcinoma and non-cardia gastric adenocarcinoma in individuals who had received H. pylori eradication treatment was compared with the background population of the corresponding age, sex and calendar year distribution, yielding standardised incidence ratios (SIRs) with 95% CIs.

Results During the follow-up of 95 176 individuals who had received eradication treatment (351 018 person-years at risk), 75 (0.1%) developed gastric adenocarcinoma and 69 (0.1%) developed non-cardia gastric adenocarcinoma. The risk of gastric adenocarcinoma decreased over time after eradication treatment to levels below that of the corresponding background population. The SIRs were 8.65 (95% CI 6.37 to 11.46) for 1–3 years, 2.02 (95% CI 1.25 to 3.09) for 3–5 years and 0.31 (95% CI 0.11 to 0.67) for 5–7.5 years after eradication treatment. When restricted to non-cardia adenocarcinoma, the corresponding SIRs were 10.74 (95% CI 7.77 to 14.46), 2.67 (95% CI 1.63 to 4.13) and 0.43 (95% CI 0.16 to 0.93).

Conclusion Eradication treatment for H. pylori seems to counteract the development of gastric adenocarcinoma and non-cardia gastric adenocarcinoma in this Western population.

  • helicobacter pylori
  • gastric cancer
  • antibiotic therapy

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Footnotes

  • Contributors Design of the study: all authors; Data collection and preparation for analyses: NB and ED; Data analysis: ED with support from NB; Data interpretation: all authors; Writing of first draft: ED, revised and approved by all authors.

  • Funding Strategic Research Area (SFO), Karolinska Institutet internal funding for doctoral education (KID funding), Swedish Society of Medicine, Swedish Research Council and Swedish Cancer Society.

  • Competing interests None declared.

  • Ethics approval The study was approved by the Regional Ethical Review Board in Stockholm (2014/1291-31/4).

  • Provenance and peer review Not commissioned; externally peer reviewed.

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