Helicobacter pylori is associated with increased risk of serrated colonic polyps: Analysis of serrated polyp risk factors
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.
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.
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).
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.
KeywordsColorectal neoplasia Helicobacter pylori Serrated polyp Sessile serrated adenoma Traditional serrated adenoma
Compliance with ethical standards
Conflict of interest
AK, MK, and DJL declare that they have no conflict of interest.
The study was performed in a manner to conform with the Helsinki Declaration of 1975, as revised in 2000 and 2008concerning human and animal rights, and the authors followed the policy concerning informed consent as shown on Springer.com. The study was approved by the Institutional Review Board at the Albert Einstein College of Medicine.
- 1.Okamoto K, Kitamura S, Kimura T, et al. Clinicopathological characteristics of serrated polyps as precursors to colorectal cancer: current status and management. J Gastroenterol Hepatol. 2017;32:358–67.Google Scholar
- 3.Iino H, Jass JR, Simms LA, et al. DNA microsatellite instability in hyperplastic polyps, serrated adenomas, and mixed polyps: a mild mutator pathway for colorectal cancer? J Clin Pathol. 1999;52:5–9.Google Scholar
- 8.Snover DCAD, Burt RW, Odze RD. Serrated polyps of the colon and rectum and serrated polyposis. In: Bosman FTCF, Hruban RH, Theise ND, Eds. WHO Classification of Tumours of the Digestive System. 4th ed. Lyon: IARC; 2010; Pp 160–5.Google Scholar
- 13.Anderson JC, Rangasamy P, Rustagi T, et al. Risk factors for sessile serrated adenomas. J Clin Gastroenterol. 2011;45:694–9.Google Scholar
- 14.Burnett-Hartman AN, Passarelli MN, Adams SV, et al. Differences in epidemiologic risk factors for colorectal adenomas and serrated polyps by lesion severity and anatomical site. Am J Epidemiol. 2013;177:625–37.Google Scholar
- 16.Breuer-Katschinski B, Nemes K, Marr A, et al. Helicobacter pylori and the risk of colonic adenomas. Digestion. 1999;60:210–5.Google Scholar
- 17.Brim H, Zahaf M, Laiyemo AO, et al. Gastric Helicobacter pylori infection associates with an increased risk of colorectal polyps in African Americans. BMC Cancer. 2014;14:296.Google Scholar
- 18.Fujimori S, Kishida T, Kobayashi T, et al. Helicobacter pylori infection increases the risk of colorectal adenoma and adenocarcinoma, especially in women. J Gastroenterol. 2005;40:887–93.Google Scholar
- 20.Wang F, Sun MY, Shi SL, Lv ZS. Helicobacter pylori infection and normal colorectal mucosa-adenomatous polyp-adenocarcinoma sequence: a meta-analysis of 27 case-control studies. Colorectal Dis. 2014;16:246–52.Google Scholar
- 21.Wu Q, Yang ZP, Xu P, Gao LC, Fan DM. Association between Helicobacter pylori infection and the risk of colorectal neoplasia: a systematic review and meta-analysis. Colorectal Dis. 2013;15:e352–64.Google Scholar
- 22.Erichsen R, Baron JA, Hamilton-Dutoit SJ, et al. Increased risk of colorectal cancer development among patients with serrated polyps. Gastroenterology. 2016;150:895–902.e5.Google Scholar
- 27.Osaki T, Matsuki T, Asahara T, et al. Comparative analysis of gastric bacterial microbiota in Mongolian gerbils after long-term infection with Helicobacter pylori. Microb Pathog. 2012;53:12–8.Google Scholar
- 29.Sonnenberg A, Turner KO, Genta RM. The ethnic distribution of sessile serrated polyps in the United States is inversely associated with Helicobacter pylori prevalence. Colorectal Dis. 2017;19:996–1002.Google Scholar
- 32.Wallace K, Brandt HM, Bearden JD, et al. Race and prevalence of large bowel polyps among the low-income and uninsured in South Carolina. Dig Dis Sci. 2016;61:265–72.Google Scholar
- 37.Omata F, Brown WR, Tokuda Y, et al. Modifiable risk factors for colorectal neoplasms and hyperplastic polyps. Intern Med. 2009;48:123–8.Google Scholar
- 38.Limsui D, Vierkant RA, Tillmans LS, et al. Cigarette smoking and colorectal cancer risk by molecularly defined subtypes. J Natl Cancer Inst. 2010;102:1012–22.Google Scholar
- 39.Wish TA, Hyde AJ, Parfrey PS, et al. Increased cancer predisposition in family members of colorectal cancer patients harboring the p.V600E BRAF mutation: a population-based study. Cancer Epidemiol Biomark Prev. 2010;19:1831–9.Google Scholar