Density of Helicobacter pylori infection evaluated semiquantitatively in gastric cancer

Citation
Y. Tokunaga et al., Density of Helicobacter pylori infection evaluated semiquantitatively in gastric cancer, J CLIN GAST, 31(3), 2000, pp. 217-221
Citations number
30
Categorie Soggetti
Gastroenerology and Hepatology
Journal title
JOURNAL OF CLINICAL GASTROENTEROLOGY
ISSN journal
01920790 → ACNP
Volume
31
Issue
3
Year of publication
2000
Pages
217 - 221
Database
ISI
SICI code
0192-0790(200010)31:3<217:DOHPIE>2.0.ZU;2-7
Abstract
Helicobacter pylori infection may play a role in the development of gastric cancer; however, a quantitative evaluation of the density of H. pylori inf ection has not been reported previously in relation to the histologic stage and type of cancer. This study was designed to compare the density of H. p ylori infection to the histologic stage and type of gastric cancer. Between March 1996 and March 1998, surgical resection of primary lesion was perfor med in 50 patients with gastric cancer (39 men and 11 women with a mean age of 67 years) at our institution. Using immunohistochemical stains, the den sity of H. pylori infection was evaluated semiquantitatively at cancer site as well as noncancerous mucosa adjacent to cancer. This density was compar ed with the histologic stage and the type of gastric cancer. The severity o f the mucosal atrophy was evaluated using the updated Sydney System. The pr evalences and density of H. pylori infection decreased in proportion to adv ances in the cancer stage and the mucosal atrophy. In early cancer of the i ntestinal- and diffuse-type, the prevalence of H. pylori in adjacent sites was almost 90% and was significantly higher (p < 0.01) than that seen in th e advanced cancer lesions. In the intestinal-type early cancer, the prevale nce and density of infection was higher (p < 0.05) in the adjacent mucosa t han in the cancer site, whereas in the diffuse-type early cancer, H. pylori was found in all cases at the cancer site and the adjacent site. In advanc ed cancer, the prevalence of H. pylori was about 40% in the adjacent site a nd about 10% in the cancer site in both histologic types. These figures wer e significantly lower (p < 0.01) than in the early cancers. The prevalence and density of infection did not differ in the intestinal- and diffuse-type gastric cancers, but did decrease with more advanced cancer stages. The ch anges in local environment of the advanced cancer may not be conducive to t he survival of H. pylori. Thus, the prevalence of H. pylori may be affected by the histologic stage rather than the histologic type of gastric cancer, and the organism may play a similar role, but through different pathways, in the pathogenesis of both types of cancer.