Helicobacter pylori is associated with increased risk of serrated colonic polyps

Analysis of serrated polyp risk factors

Anand Kumar, Mimi Kim, Dana J. Lukin

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalIndian Journal of Gastroenterology
DOIs
StateAccepted/In press - Jun 7 2018

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Colonic Polyps
Polyps
Helicobacter pylori
Adenoma
Helicobacter Infections
Neoplasms
Stomach
Smoking
Colonoscopy

Keywords

  • Colorectal neoplasia
  • Helicobacter pylori
  • Serrated polyp
  • Sessile serrated adenoma
  • Traditional serrated adenoma

ASJC Scopus subject areas

  • Gastroenterology

Cite this

@article{4f3ceb8c63144422aa1ba5bee391f010,
title = "Helicobacter pylori is associated with increased risk of serrated colonic polyps: Analysis of serrated polyp risk factors",
abstract = "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",
author = "Anand Kumar and Mimi Kim and Lukin, {Dana J.}",
year = "2018",
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doi = "10.1007/s12664-018-0855-8",
language = "English (US)",
pages = "1--8",
journal = "Indian Journal of Gastroenterology",
issn = "0254-8860",
publisher = "Indian Society of Gastroenterology",

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T1 - Helicobacter pylori is associated with increased risk of serrated colonic polyps

T2 - Analysis of serrated polyp risk factors

AU - Kumar, Anand

AU - Kim, Mimi

AU - Lukin, Dana J.

PY - 2018/6/7

Y1 - 2018/6/7

N2 - 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.

AB - 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.

KW - Colorectal neoplasia

KW - Helicobacter pylori

KW - Serrated polyp

KW - Sessile serrated adenoma

KW - Traditional serrated adenoma

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