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Gastric Cancer Precursor Lesions and Helicobacter pylori Infection in Patients with Partial Gastrectomy for Peptic Ulcer

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Abstract

The mucosa of the gastric stump is considered at greater risk of dysplastic and neoplastic changes than that of the intact stomach. The combination of enteric reflux and Helicobacter pylori infection may have a synergistic damaging effect on the mucosa of the gastric remnant, both producing and increasing mucosal proliferation. The aim of this study was to assess whether the occurrence of H. pylori infection in the remnant mucosa of partially gastrectomized subjects for peptic ulcer disease is associated with an increase of the mucosal precursor lesions of malignancy. A series of 151 subjects who underwent partial gastrectomy for peptic ulcer disease were submitted to upper digestive endoscopy for long-term surveillance. Biopsy specimens of the gastric stump were tested for the occurrence of H. pylori infection and for the presence of precancerous mucosal lesions. The prevalence of H. pylori colonization in the remnant stomach was less than 30% and similar in subjects with different time intervals between gastrectomy and endoscopy. Age at surgery (χ2: p = 0.03) and H. pylori infection (χ2: p = 0.002) were significantly associated with the grading of mucosal lesions. The prevalence of normal mucosa was 10 times higher in H. pylori-negative patients as in H. pylori-positive ones (22.0% vs. 2.4%), and the prevalence of intestinal metaplasia was four times higher in H. pylori-positive patients than in H. pylori-negative ones (19.6% vs. 4.6%). We concluded that H. pylori infection may play a causal role in the development of gastric lesions in the operated stomach.

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Correspondence to Francesco Angelico M.D..

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Giuliani, A., Caporale, A., Demoro, M. et al. Gastric Cancer Precursor Lesions and Helicobacter pylori Infection in Patients with Partial Gastrectomy for Peptic Ulcer. World J. Surg. 29, 1127–1130 (2005). https://doi.org/10.1007/s00268-005-7713-4

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  • DOI: https://doi.org/10.1007/s00268-005-7713-4

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