Gut 61:812-818 doi:10.1136/gutjnl-2011-300154
  • Stomach
  • Original article

Effects of selective COX-2 inhibitor and Helicobacter pylori eradication on precancerous gastric lesions

  1. Wei-cheng You2
  1. 1Department of Medicine, University of Hong Kong, Hong Kong, China
  2. 2The Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Cancer Epidemiology, Peking University Cancer Hospital & Institute, Beijing, China
  3. 3Department of Pathology, Peking University Cancer Hospital & Institute, Beijing, China
  4. 4Department of Medical Oncology, Peking University Cancer Hospital & Institute, Beijing, China
  5. 5Healthy Bureau of Linqu County, Shandong, China
  1. Correspondence to Wei-cheng You, The Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Peking University Cancer Hospital & Institute, 52 Fu-cheng Road, Hai-dian District, Beijing 100142, China; weichengyou{at}
  1. Contributors All authors directly participated in the planning, execution, or analysis of the study. All authors have read and approved the final version submitted. All authors accept responsibility for its content. Study organisation was by WY, and BCYW designed the study. WY, BCYW, LZ and SL supervised the execution of the study. LZ, JM, KP, WL and HHXX were responsible for the field administration and data collection. LS, XZ and JL were responsible for the endoscopic examination. J-yL and AL were responsible for the pathological diagnosis. GF and KP performed the statistical analyses. WY, LZ, KP and BCYW drafted the manuscript.

  • Revised 31 July 2011
  • Accepted 11 August 2011
  • Published Online First 13 September 2011


Objective Helicobacter pylori infection and overexpression of cyclo-oxygenase-2 (COX-2) are associated with gastric cancer and its precursors. To evaluate the effect of a selective COX-2 inhibitor alone and combined with H pylori eradication on the evolution of precancerous gastric lesions, a randomised, placebo-controlled trial was conducted in Linqu County, Shandong Province, China.

Methods A total of 1024 participants aged 35–64 years with H pylori infection and advanced gastric lesions were randomly assigned in a factorial design to two interventions or placebo: anti-H pylori treatment for 7 days, and a COX-2 inhibitor (celecoxib) for 24 months. The effects of the interventions were evaluated by the regression or progression of advanced gastric lesions.

Results Of the 1024 participants who received anti-H pylori treatment or placebo, 919 completed a subsequent 24-month treatment with celecoxib or placebo. The H pylori eradication rate by per-protocol analysis was 78.2%. Compared with placebo, the proportions of regression of gastric lesions significantly increased in the celecoxib treatment (52.8% vs 41.2%) and anti-H pylori treatment (59.3% vs 41.2%) group, and OR by per-protocol analysis was 1.72 (95% CI 1.07 to 2.76) for celecoxib and 2.19 (95% CI 1.32 to 3.64) for H pylori eradication. No statistically significant effect was found for H pylori eradication followed by celecoxib on the regression of advanced gastric lesions (OR 1.48, 95% CI 0.91 to 2.40).

Conclusion This population-based intervention trial revealed that celecoxib treatment or H pylori eradication alone had beneficial effects on the regression of advanced gastric lesions. No favourable effects were seen for H pylori eradication followed by celecoxib treatment.

Trial registration HARECCTR0500053 in accordance with WHO ICTRP requirements.


  • BCYW and LZ contributed equally to this article.

  • Funding This study was supported in part by grants from National High Technology R&D Program (2006AA02A402), National Basic Research Program of China (973 Program, 2010CB529303), National Natural Science Foundation (30471957, 30772515), a grant from Peking University and the Earmarked Research Grant from the Research Grant Council, Hong Kong (Project code: HKU 7256/01M).

  • Competing interests None.

  • Patient consent Obtained.

  • Ethics approval The project was approved by the institutional review board of Peking University School of Oncology (PUSO) and University of Hong Kong (EC-1721-01).

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

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