Helicobacter pylori in promotion of gastric carcinogenesis |
| |
| Authors: | Dr. Massimo Rugge MD Mauro Cassaro MD Gioacchino Leandro MD Raffaele Baffa MD Claudio Avellini MD Pantaleone Bufo MD Vincenzo Stracca MA Giuseppe Battaglia MD Alfredo Fabiano MD Antonio Guerini MD Francesco di Mario MD |
| |
| Affiliation: | (1) From the Department of Pathology, University of Padova-ULSS, 15 Veneto Region, Italy;(2) Gastroenterology Hospital DeBellis, Castellana Grotte (BA), Italy;(3) Department of Pathology, University of Udine, Italy;(4) Department of Pathology, University of Bari, Italy;(5) Departments of Pathology and Internal Medicine, Venice Hospital, Italy;(6) Department of Pathology, Fatebenefratelli Hospital, Rome;(7) Department of Pathology, Bassano Hospital (VI), Italy;(8) Department of Gastroenterology, University of Padua, Paudua, Italy;(9) Department of Pathology, University of Padua, Via A. Gabelli 61, I-35121 Padua, Italy |
| |
| Abstract: | Gastric atrophy and intestinal metaplasia are considered the earliest phenotypic changes in the cascade of events leading from normal mucosa to intestinal-type gastric cancer, and epidemiological evidence linksHelicobacter pylori to gastric epithelial malignancies. To evaluate any causal relationship between bacterial infection and atrophic metaplastic lesions, gastric pathology was histologically and histochemically evaluated in 267 consecutive, nonulcerous, untreated subjects, with attention given to the phenotypes of intestinal metaplasia. The prevalence ofHelicobacter pylori infection was 61%. Intestinal metaplasia (particularly types II and III) was significantly associated with bothHelicobacter pylori detection (xLR2:P<0.002) and increasing age (xLR2:P<0.002). Using logistic regression analysis, the development of intestinal metaplasia proved more significantly linked withHelicobacter pylori infection [odds ratio=4.55 (95% confidence interval: 1.51–13.7)], than with age [odds ratio =1.03 (95% CI: 1.01–1.06)], with no interaction. In conclusion,Helicobacter pylori can be considered among the major causal agents of mucosal lesions involved in the multistep process of gastric carcinogenesis, justifying any attempt to eradicate this bacterial infection. |
| |
| Keywords: | Helicobacter pylori intestinal metaplasia gastric precancer mucin histochemistry atrophic gastritis multifocal atrophic gastritis |
| 本文献已被 SpringerLink 等数据库收录！ |
|
