BACKGROUND: Although E-cadherins have been involved in gastric carcinogenesis, their role in precancerous lesions, such as intestinal metaplasia, is still unclear. This study aimed to assess the role of both intestinal metaplasia and H. pylori infection on E-cadherin expression in gastric mucosa. PATIENTS AND METHODS: Twenty-one consecutive patients with intestinal metaplasia were enrolled to assess E-cadherin expression in metaplastic areas. Twenty further patients without intestinal metaplasia, with and without H. pylori, were enrolled to evaluate the role of the infection on E-cadherin expression. All patients underwent upper endoscopy and gastric biopsies were taken for histological and immunohistochemical assessment. RESULTS: A substantial reduction of E-cadherin expression in metaplastic areas was observed in 14 (67%) of the 21 patients, similarly in H. pylori-infected and uninfected patients (64% vs 71%, p=0.3). In the group without intestinal metaplasia, no reduction in E-cadherin expression was detected either in infected patients or in those without H. pylori infection. CONCLUSION: The data showed that intestinal metaplasia is associated with E-cadherin down-regulation, whereas H. pylori infection does not seem to play a direct role in this process.
BACKGROUND: Although E-cadherins have been involved in gastric carcinogenesis, their role in precancerous lesions, such as intestinal metaplasia, is still unclear. This study aimed to assess the role of both intestinal metaplasia and H. pyloriinfection on E-cadherin expression in gastric mucosa. PATIENTS AND METHODS: Twenty-one consecutive patients with intestinal metaplasia were enrolled to assess E-cadherin expression in metaplastic areas. Twenty further patients without intestinal metaplasia, with and without H. pylori, were enrolled to evaluate the role of the infection on E-cadherin expression. All patients underwent upper endoscopy and gastric biopsies were taken for histological and immunohistochemical assessment. RESULTS: A substantial reduction of E-cadherin expression in metaplastic areas was observed in 14 (67%) of the 21 patients, similarly in H. pylori-infected and uninfected patients (64% vs 71%, p=0.3). In the group without intestinal metaplasia, no reduction in E-cadherin expression was detected either in infectedpatients or in those without H. pyloriinfection. CONCLUSION: The data showed that intestinal metaplasia is associated with E-cadherin down-regulation, whereas H. pyloriinfection does not seem to play a direct role in this process.