This study evaluates whether Helicobacter pylori eradication improves precancerous lesions including glandular atrophy and intestinal metaplasia as well as metachronous cancers or dysplasias after endoscopic mucosal resection for gastric cancer.
Helicobacter pylori is a primary etiological agent leading to chronic gastritis and peptic ulcer. The organism is also associated with gastric cancer in epidemiological studies. However detailed mechanism of carcinogenesis remains unknown. Histolopathological studies indicate that chronic H. pylori infection progresses over decades through stages of chronic gastritis, atrophy, intestinal metaplasia, dysplasia and cancer. Gastric atrophy and intestinal metaplasia are considered as precancerous lesions, but whether H. pylori eradication improves these lesions and prevents metachronous gastric cancer is controversial. And the issue has not been evaluated in gastric cancer patients. However, despite the conflicting evidences from two open labelled randomized controlled trials, current guidelines from various regions recommend H. pylori eradication treatment in patients who were treated for gastric cancer by surgically or endoscopically. Thus, it is important to evaluate whether H. pylori eradication can improve known precancerous lesion, i.e. glandular atrophy and intestinal metaplasia in gastric cancer patients. Such histological improvement can eventually reduce secondary gastric cancer development and provide evidence for current guidelines.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
QUADRUPLE
Enrollment
470
Omeprazole 20 mg or Rabeprazole 10 mg bid for 7 days, Clarithromycin 500 mg bid for 7 days, Amoxicillin 1,000 mg bid for 7 days.
Omeprazole 20 mg or Rabeprazole 10 mg bid for 7 days, Placebo for clarithromycin 500 mg bid for 7 days, Placebo for amoxicillin 1,000 mg bid for 7 days.
National Cancer Center, Korea
Goyang-si, Gyeonggi-do, South Korea
Improvement (histological) of glandular atrophy
Improvement of glandular atrophy at the corpus lesser curvature
Time frame: 3 years after enrollment
Incidence of metachronous gastric cancer
Comparison of metachronous gastric cancer according to the allocated treatment
Time frame: 3 years after last patient enrollment
Incidence of new gastric dysplasia
Comparison of new gastric dysplasia according to the allocated treatment
Time frame: 3 years after last patient enrollment
Overall survival
Comparison of overall survival according to the allocated treatment
Time frame: 3 years after last patient enrollment
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