Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases

Susumu Take, Motowo Mizuno, Kuniharu Ishiki, Yasuhiro Nagahara, Tomowo Yoshida, Kenji Yokota, Keiji Oguma

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

Background: We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient groups to identify factors associated with the development of gastric cancer. Methods: Prospective posteradication evaluations were conducted in 1342 consecutive patients (1191 men and 151 women; mean age, 50 years) with peptic ulcer disease who had received H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosa, and H. pylori infection. After confirmation of eradication, follow-up endoscopy was performed yearly. Results: A total of 1131 patients were followed for up to 9.5 years (mean, 3.9 years). Gastric cancer developed in 9 of 953 patients cured of infection and in 4 of 178 who had persistent infection (P = 0.04). The risk of developing gastric cancer after receiving H. pylori eradication therapy was increased according to the grade of baseline gastric mucosal atrophy (P = 0.01). In patients with peptic ulcer diseases, persistent infection of H. pylori (hazard ratio, 3.9; P = 0.03), the grade of baseline gastric mucosal atrophy (3.3, P = 0.01) and age (2.0, P = 0.04) were identified as significant risk factors for developing gastric cancer. Conclusions: The grade of gastric atrophy was closely related to the development of gastric cancer after receiving H. pylori eradication therapy. Thus, eradication of H. pylori before the significant expansion of atrophy is most beneficial to prevent gastric cancer.

Original languageEnglish
Pages (from-to)21-27
Number of pages7
JournalJournal of Gastroenterology
Volume42
Issue numberSUPPL.17
DOIs
Publication statusPublished - Jan 2007

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Peptic Ulcer
Helicobacter pylori
Stomach Neoplasms
Atrophy
Stomach
Therapeutics
Infection
Helicobacter Infections
Gastric Mucosa
Endoscopy

Keywords

  • Eradication therapy
  • Gastric cancer
  • Gastric mucosal atrophy
  • Helicobacter pylori
  • Peptic ulcer disease

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases. / Take, Susumu; Mizuno, Motowo; Ishiki, Kuniharu; Nagahara, Yasuhiro; Yoshida, Tomowo; Yokota, Kenji; Oguma, Keiji.

In: Journal of Gastroenterology, Vol. 42, No. SUPPL.17, 01.2007, p. 21-27.

Research output: Contribution to journalArticle

Take, Susumu ; Mizuno, Motowo ; Ishiki, Kuniharu ; Nagahara, Yasuhiro ; Yoshida, Tomowo ; Yokota, Kenji ; Oguma, Keiji. / Baseline gastric mucosal atrophy is a risk factor associated with the development of gastric cancer after Helicobacter pylori eradication therapy in patients with peptic ulcer diseases. In: Journal of Gastroenterology. 2007 ; Vol. 42, No. SUPPL.17. pp. 21-27.
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AU - Take, Susumu

AU - Mizuno, Motowo

AU - Ishiki, Kuniharu

AU - Nagahara, Yasuhiro

AU - Yoshida, Tomowo

AU - Yokota, Kenji

AU - Oguma, Keiji

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N2 - Background: We previously reported that eradication of Helicobacter pylori could reduce the risk of developing gastric cancer in patients with peptic ulcer diseases. In the present study, we further followed up our patient groups to identify factors associated with the development of gastric cancer. Methods: Prospective posteradication evaluations were conducted in 1342 consecutive patients (1191 men and 151 women; mean age, 50 years) with peptic ulcer disease who had received H. pylori eradication therapy. The patients had undergone endoscopic examination before eradication therapy to evaluate peptic ulcers, background gastric mucosa, and H. pylori infection. After confirmation of eradication, follow-up endoscopy was performed yearly. Results: A total of 1131 patients were followed for up to 9.5 years (mean, 3.9 years). Gastric cancer developed in 9 of 953 patients cured of infection and in 4 of 178 who had persistent infection (P = 0.04). The risk of developing gastric cancer after receiving H. pylori eradication therapy was increased according to the grade of baseline gastric mucosal atrophy (P = 0.01). In patients with peptic ulcer diseases, persistent infection of H. pylori (hazard ratio, 3.9; P = 0.03), the grade of baseline gastric mucosal atrophy (3.3, P = 0.01) and age (2.0, P = 0.04) were identified as significant risk factors for developing gastric cancer. Conclusions: The grade of gastric atrophy was closely related to the development of gastric cancer after receiving H. pylori eradication therapy. Thus, eradication of H. pylori before the significant expansion of atrophy is most beneficial to prevent gastric cancer.

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