Helicobacter Pylori Infection Is an Independent Risk Factor for Development of Serrated Colonic Polyps: A Retrospective Analysis

Abstract

Introduction: Serrated colonic polyps (SPs) are classified into hyperplastic polyps (HP), sessile serrated adenomas (SSA) and traditional serrated adenomas (TSA). SSA & TSA are now recognized as precancerous lesions for colorectal cancer (CRC). Studies have found a positive association between Helicobacter pylori infection (HPI) and the risk of colorectal adenoma and CRC. We investigated this association with SPs. Methods: Using our institutional computerized database we identified patients aged ≥18 years who underwent colonoscopic biopsies between 2005 & 2015. Based on the histological diagnosis they were divided into study group: patients with SP (SSA & TSA but not HP) and control group: patients with polyps without serrated features and no SP diagnosed in 20 years around the index date. Given the possibility of HP with unreported serrated features in this group, we created two more control groups: patients with adenomatous polyp (AP) without HP or SP; patients with no polyp on histology (not including patients with colonoscopy but no biopsies taken). Prior 10 years' records were explored for all groups to capture an exposure to HPI, defined by the identification of HPI by Warthin-Starry staining on gastric biopsy or by a positive stool antigen or urea breath test. Exposure risk was compared using crude and adjusted odds ratios (OR).Table 1: Characteristics of the Study Cohort (Patients with Serrated Polyps)Table 2a: Frequency of Exposure in Different GroupsTable 2b: Association of H . pylori Exposure with Different Polyp OutcomesResults: Characteristics of the study group are listed in table 1. The frequency of HPI in each group is described in table 2a. The highest period-prevalence of HPI (11/100 patients) was seen in Hispanic females with SP and below average socioeconomic status (SES), and the lowest ( < 1/100 patients) was in white men with no polyp. Adjusted ORs indicated that HPI increased the risk of SP as compared to any other polyp type or no polyp, independent of age, gender, race and SES (table 2b). On multiple regression analysis of SP vs. non-serrated polyp, besides exposure to HPI, older age (OR 1.009; 95% CI 1.004-1.014), female gender (OR 1.17; 95% CI 1.03-1.32), smoking (OR 1.47; 95% CI 1.31-1.65), and higher BMI (OR 1.010; 95% CI 1.001-1.019) increased the risk of developing SP. Though lower SES was associated with higher prevalence of HPI, it did not independently increase the risk of SP. Conclusion: HPI is associated with increased risk of developing SPs (SSA & TSA) when compared to patients without SP, AP (without SP and HP), and without colonic polyps. Prospective studies are required to confirm a causal relationship between HPI and SP.