OBJECTIVE: This prospective cohort study investigated the impact of Helicobacter pylori infection on the development of various gastric malignancies. METHODS: We prospectively followed up 1,225 dyspeptic Taiwanese who had nonulcer dyspepsia, gastric ulcers, or duodenal ulcers at enrollment. Among them, 618 (50.4%) had H. pylori infection and 607 (49.6%) did not. Patients underwent endoscopy at enrollment and at 1- to 3-yr intervals thereafter. RESULTS: During a mean follow-up of 6.3 yr, gastric adenocarcinoma developed in 7 of the 618 H. pylori-infected patients, but in none of the 607 uninfected patients (1.1%vs 0.0%, P= 0.015). The incidence of gastric lymphoma was 0.2% (1/618) and 0% in H. pylori-infected and uninfected patients. Taken together, the development rate of gastric malignancy in H. pylori-infected patients was significantly higher than that in uninfected patients (1.3%vs 0%, P= 0.007). Among H. pylori-infected subjects, the incidence of gastric malignancy was similar between those receiving and not receiving eradication therapy (1.4%vs 1.2%). Multivariate analysis showed that intestinal metaplasia was the only independent factor predicting subsequent development of gastric malignancy in H. pylori-infected subjects with an odds ratio of 4.5 (95% CI 1.1-19.1). CONCLUSIONS: In this prospective cohort study, all gastric malignancies, including adenocarcinoma and lymphoma, developed in H. pylori-infected patients. The finding implies that H. pylori is a necessary cause of most gastric malignancies. Follow-up for H. pylori-infected patients who have intestinal metaplasia is indicated.
OBJECTIVE: This prospective cohort study investigated the impact of Helicobacter pyloriinfection on the development of various gastric malignancies. METHODS: We prospectively followed up 1,225 dyspeptic Taiwanese who had nonulcer dyspepsia, gastric ulcers, or duodenal ulcers at enrollment. Among them, 618 (50.4%) had H. pyloriinfection and 607 (49.6%) did not. Patients underwent endoscopy at enrollment and at 1- to 3-yr intervals thereafter. RESULTS: During a mean follow-up of 6.3 yr, gastric adenocarcinoma developed in 7 of the 618 H. pylori-infectedpatients, but in none of the 607 uninfected patients (1.1%vs 0.0%, P= 0.015). The incidence of gastric lymphoma was 0.2% (1/618) and 0% in H. pylori-infected and uninfected patients. Taken together, the development rate of gastric malignancy in H. pylori-infectedpatients was significantly higher than that in uninfected patients (1.3%vs 0%, P= 0.007). Among H. pylori-infected subjects, the incidence of gastric malignancy was similar between those receiving and not receiving eradication therapy (1.4%vs 1.2%). Multivariate analysis showed that intestinal metaplasia was the only independent factor predicting subsequent development of gastric malignancy in H. pylori-infected subjects with an odds ratio of 4.5 (95% CI 1.1-19.1). CONCLUSIONS: In this prospective cohort study, all gastric malignancies, including adenocarcinoma and lymphoma, developed in H. pylori-infectedpatients. The finding implies that H. pylori is a necessary cause of most gastric malignancies. Follow-up for H. pylori-infectedpatients who have intestinal metaplasia is indicated.
Authors: Erin C Bridgeford; Robert P Marini; Yan Feng; Nicola M A Parry; Barry Rickman; James G Fox Journal: Vet Immunol Immunopathol Date: 2008-01-19 Impact factor: 2.046