28 Background: Atrophic gastritis and intestinal metaplasia were considered as premalignant lesions. The prevalence of chronic atrophic gastritis is very high in Korea. The aims of this study were to evaluate the risk factors of gastric carcinogenesis in underlying gastric mucosal atrophy. Methods: A total of 10187 subjects underwent upper gastrointestinal endoscopy for health checkup between 2003 and 2004 were enrolled in this retrospective cohort study. Follow-up endoscopy was performed between 2005 and 2014. Atrophic gastritis and intestinal metaplasia were assessed according to the Kimura-Takemoto classification by endoscopy. Helicobacter pylori (Hp) was evaluated by serum IgG antibody. Results: The number of atrophic gastritis was 3716 (36.5%) in baseline endoscopy, and 2146 were undergone follow-up endoscopy (82.8±38.3month); 1139 showed aggravation of atrophy and 1007 showed no change. A total of 71 subjects were diagnosed as gastric neoplasms (34 adenoma, 37 carcinoma). Age (HR = 1.019, 95%CI 1.010-1.028), alcohol intake (HR = 1.002, 95%CI 1.001-1.002), Salt intake (HR = 1.295, 95%CI 1.038-1.617) and Hp infection (HR = 1.584, 95%CI 1.220-2.057) were associated with aggravation of mucosal atrophy. The risk factors for gastric neoplasm in underlying mucosal atrophy were age (HR = 1.041, 95%CI 1.004-1.079), alcohol intake (HR = 1.003, 95% CI 1.001-1.005), Salt intake (HR = 2.553, 95% CI 1.141-5.712), Extent of mucosal atrophy (HR = 2.375, 95% CI 1.201-4.695 in C3-O1; HR = 4.255, 95% CI 1.612-11.229 in O2-O3), and intestinal metaplasia (HR = 2.599, 95% CI 1.286-5.251). Conclusions: Hp was a risk factor for aggravation of atrophy, but not for gastric neoplasm. Salt intake, extent of mucosal atrophy, and intestinal metaplasia were important risk factors for gastric neoplasm.
Is intestinal metaplasia the point of no return in the progression of gastric carcinogenesis?
