Helicobacter pylori-Negative Advanced Gastric Cancer Arising from the Gastric Mucosa without Inflammation, Atrophy, or Intestinal Metaplasia

Abstract

Gastric cancer is strongly associated with atrophic gastritis associated with Helicobacter pylori infection. The eradication of H. pylori has been reported to improve inflammation of the gastric mucosa, atrophy, and intestinal metaplasia and has also been shown to inhibit the development and growth of gastric cancer. Advanced gastric cancer from H. pylori-negative mucosa without inflammation, atrophy, or intestinal epithelialization is rarely found. We report on two cases of advanced gastric cancer without endoscopic evidence of gastric mucosal atrophy. One case was in the gastric angle 9 years after H. pylori eradication and the other case was in the pylorus of an uninfected stomach. Although gastric cancer is strongly associated with atrophic gastritis caused by H. pylori infection, postoperative histopathological examination of the stomach in both cases showed no inflammation, atrophy, or intestinal metaplasia. Poorly differentiated adenocarcinomas were confirmed at the microscopic level, and both cases were determined to be type 4 using the Borrmann classification. There is a body of evidence showing that H. pylori infection can cause gastric cancer and is the most prevalent infection-induced cancer in the world. The 2 cases here displayed different carcinogenesis than gastric mucosal atrophy caused by H. pylori infection. With the spread of H. pylori eradication treatments and an increasing number of uninfected patients, these case reports can contribute to future strategies for the diagnosis of gastric cancer.

Keywords: Atrophic gastritis; Carcinogenesis; Endoscopy; Gastric cancer; Helicobacter pylori infection.

Fig. 1

Endoscopic findings and histopathological findings of the resected stomach of case 1. An ulcerative lesion with sclerosis was found on the posterior wall of the gastric angle (a, b). There were no atrophic changes in the pyloric (c) or corpus mucosa (d), suggesting an apparently uninfected stomach. The tumor cells invaded the serosa with marked fibrosis (e). There was a diffuse intramucosal growth of undifferentiated tumor cells (f). Histopathological findings of the mucosa in the pyloric (g) and fundic gland regions (h) showed no inflammation, no mucosal atrophy, and no intestinal metaplasia (e–h: H&E staining, (e): 2 × 10, (f–h): 20 × 10).

Fig. 2

Endoscopic findings and histopathological findings of the resected stomach of case 2. A drainage tube was inserted due to the pyloric stenosis (a). There was a circumferential stenosis in the pylorus, with ring-shaped mucosal folds in the proximal view and ulceration in some areas (b). The mucosa of the angle and gastric body in front of the stenosis did not show any atrophic changes, such as vascular permeability (c, d). Undifferentiated tumor cells proliferated mainly in the submucosa (e), with marked fibrosis, and invaded the serosa (f). Histopathological findings of the mucosa in the pyloric (g) and gastric fundic glands (h) showed no inflammation, no atrophy, and no intestinal metaplasia (e–h: H&E staining (e): 2 × 10, (f): 40 × 10, (g, h): 20 × 10).