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

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 (chi(2): p = 0.03) and H. pylori infection (chi(2): 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.

Behavior of the Infection by Helicobacter pylori of the Gastric Remnant After Subtotal Gastrectomy and Roux-en-Y Anastomosis for Benign Diseases

“…Previous studies are very few and have the same problems: (a) The majority of the publications are related to partial gastrectomy after early or advanced cancer, 1,2,[4][5][6][7]12 (b) all studies refer to only one endoscopy and biopsy samples after surgery, and (c) the majority of the studies are done 3 to 12 months after surgery, and very few have been performed years after surgery for benign diseases. 3,4,13 We have tried to overcome some of the difficulties. First, we performed a prospective consecutive evaluation before and late after surgery in a homogenous group of patients with benign disease.…”

“…7 Even some authors have postulated that H. pylori is responsible of the appearance of cancer of the gastric remnant late after surgery. 3,4 Giuliani et al 3 performed in 151 gastrectomized patients an endoscopic and histologic study 25 years after surgery. They found 29% of H. pylori infection after Billroth II and postulate that both H. pylori and enterogastric reflux may have a synergistic causal role in the development of gastric cancer.…”

HELICOBACTER PYLORI INFECTION AND TREATMENT OUTCOME IN AN URBAN AUSTRALIAN POPULATION

“…They have recently been awarded the Nobel Prize in Medicine for their discovery 5 . It is now accepted that H. pylori causes chronic gastritis, peptic ulcer disease and gastric adenocarcinoma 3,4,22–28 . H. pylori infection may be the most common chronic bacterial infection worldwide 29 .…”

“…Twenty‐nine per cent of our patients had positive UBT after initial triple therapy. Confirmation of H. pylori eradication after treatment is recommended as it reassures the patient and prevents potential future complications such as recurrent peptic ulcer disease or potentially gastric adenocarcinoma 23–28,59–64 . It also directs further management such as re‐treatment in H. pylori eradication failure or switch to symptomatic therapy 49–51,56,57 .…”

Risk of Upper Gastrointestinal Cancer after Bariatric Operations

“…4,7 The prevalence of HP after partial gastrectomy is <50% and might be influenced by duodenogastric reflux. 8 This bacterium has not been found to be specific in the patients presenting with dysplasia or adenocarcinoma of the gastric remnant, but in the endoscopic surveillance study after partial gastrectomy of Giuliani et al, 9 the prevalence of intestinal metaplasia was four times higher in HPpositive patients (19.6% vs 4.6%). Ebstein-Barr virus was also suggested as a potential co-factor by Yamamoto 10 et al associated with gastric remnant cancer after partial gastrectomy.…”