Background: Sessile serrated adenomas (SSA) and traditional serrated adenomas (TSA) are recognized precursors of colorectal cancer, but their risk factors are not well established. We investigated the association between Helicobacter pylori infection (HPI) and the development of SSA and TSA.
Methods: Retrospective data were collected on patients aged ≥ 18 years that underwent colonoscopy with biopsy between 2006 and 2016. Based on histology, patients were classified into three groups: those with SSA and/or TSA, (serrated neoplasia group, SN); conventional adenomas only (CA); and with no polyps (NP). Gastric HPI status, demographic, and clinical risk factors were compared between groups using bivariate and multivariable analysis.
Results: HPI was significantly associated with increased risk of SN (SN vs. NP: OR 1.71 [95% CI 1.29-2.27]; SN vs. CA: 1.49 [1.14-1.96]). Additional factors associated with increased risk of SN included the following: age 50-75 years, compared to younger age (SN vs. NP: 2.83 [1.69-4.74]), female gender (SN vs. CA: 1.28 [0.99-1.64]), White race, compared to Blacks (SN vs. CA: 1.52 [1.07-2.15)], overweight and obese body mass index [SN vs. NP: p < 0.001) and current smoking status (SN vs. CA: 2.09 [1.55-2.82)]. Among SN, higher HPI prevalence was associated with dysplasia (p = 0.05) and proximal location (p = 0.01).
Conclusions: Our data suggest that gastric HPI is associated with increased risk of SN and CA, with a stronger association with SN as compared to CA. Age 50-75 years, female gender, White race, obesity, and smoking were also predictors of SN. A positive correlation of HPI with proximal and dysplastic SN suggests a possible role in serrated pathway carcinogenesis. Prospective studies with large patient population are needed to further investigate this association.
Keywords: Colorectal neoplasia; Helicobacter pylori; Serrated polyp; Sessile serrated adenoma; Traditional serrated adenoma.