278 Helicobacter pylori Infection History Is Not a Risk Factor for Metachronous Advanced Adenoma: 8 Years' Follow-Up Study

Abstract

INTRODUCTION: There have been several studies suggesting the association between Helicobacter pylori. (H. pylori) infection and colorectal adenoma or cancer. However, this causal relationship is still controversial. Most atrophic gastritis (AG) is caused by H. pylori infection and can be used as surrogate marker of H. pylori infection history. On the other hand, advanced adenoma (adenoma more than 10 mm or high-grade dysplasia (HGD) or villous adenoma) has been used as surrogate marker for risk evaluation of colorectal adenocarcinoma. The aim of this study was to determine the association between H. pylori infection and post-colonoscopy advanced adenoma (PCAA). METHODS: A retrospective cohort study was conducted in a center of preventive medicine and affiliated tertiary referral center in Tokyo, Japan. Consecutive 3104 individuals had general health check-up including esophagogastroduodenoscopy (EGD) between April 2004 and July 2014 and underwent initial diagnostic or screening colonoscopy within six months after general health check-up. The patients with history of inflammatory bowel disease or colectomy or only index colonoscopy were excluded. Baseline data included age, gender, height, weight, smoking history, index colonoscopy findings (the number of adenoma, maximum size of adenoma, HGD, villous adenoma), and EGD findings (AG). To determine the longitudinal association between baseline AG and PCAA, we calculated Kaplan-Meier estimates within eight years' horizon and performed multivariate Cox proportional hazards regression. RESULTS: Mean age [SD] of 3104 patients was 55 [12] years-old and 2169 patients (70%) were male. Mean BMI [SD] was 23 [3.2]. 1188 (39%) patients were diagnosed with AG. At the index colonoscopy, 1310 patients (42%) were diagnosed with colorectal adenoma. The cumulative incidence [95%CI] of PCAA at 3, and 5 years in the patients with AG was 3% [2–5], and 8% [6–10], respectively. Crude hazard ratio (HR) [95% CI] of age, male gender, body mass index, current smoking, and AG was 1.03 [1.02–1.05], 1.35 [0.9–2.03], 1.04 [0.98–1.1], 1.5 [0.98–2.27], and 1.46 [1.02–2.1]. Adjusted HR [95% CI] of age, current smoking, AG was 1.03 [1.02–1.05], 1.6 [1.04–2.5], and 1.2 [0.85–1.8], respectively. CONCLUSION: Older age and current smoking were significant risk factors of PCAA, but AG was not. The association between AG (H. pylori infection history) and PCAA was confounded by age and current smoking. The causal relationship between H. pylori infection and PCAA was not supported by our study.