Abstract
Aim. The aim of the paper is to determine association between H. pylori and colonic adenomatous polyps and to explore whether treatment or chronic PPI use can mitigate this risk. Methods. This case-control study included 943 patients who had H. pylori testing and underwent colonoscopy. Presence of polyps was the outcome of interest, whereas age, sex, race, H. pylori infection, triple therapy, and chronic PPI use were independent variables. Multivariate regression analysis was used to calculate odds ratios at 95% confidence intervals. This study was approved by the New York Medical College Institutional Review Board. Results. H. pylori was associated with increased odds of colonic adenomatous polyps (adjusted OR 1.43, 95% CI 1.04–1.77), with stronger association among patients older than 50 (OR 1.65, 95% CI 1.18–2.33). Triple therapy (OR 0.69, 95% CI 0.44–1.07) or chronic PPI use (OR 0.69, 95% CI 0.43–1.09) decreased odds of polyp formation. Analysis revealed a statistically significant reduction in patients who received both triple therapy and chronic PPI, lowering the odds by 60% (adjusted OR 0.43, 95% CI 0.27–0.67). Conclusion. There is increased risk of colonic adenomatous polyps among H. pylori-infected patients. Triple therapy or chronic PPI use may mitigate this risk, with further reduction when these two interventions are combined.
Highlights
Helicobacter pylori (H. pylori) is a bacterium which is indigenous to humans and it is estimated that at least half of the world’s population is infected with it [1]
The authors want to determine if the presence of H. pylori infection correlates with an increased likelihood of colonic adenomatous polyp formation
We wanted to ascertain whether chronic pump inhibitor (PPI) use had an influence on the incidence of adenomatous polyp formation
Summary
Helicobacter pylori (H. pylori) is a bacterium which is indigenous to humans and it is estimated that at least half of the world’s population is infected with it [1]. Males are affected as females [2]. It has been recognized by the International Agency for Research on Cancer as a class I human carcinogen due to its ability to induce gastric adenocarcinoma. Previous investigations linking H. pylori to extragastric cancer have reported finding Helicobacter DNA in 52.6% of hepatobiliary cancer cases [4], prompting investigators to explore the hypothesis that H. pylori may be associated with intestinal polypoid structures and/or colorectal carcinoma. The presence of H. pylori has been linked with a prolonged and excessive release of gastrin [5], a hormone shown to promote the growth of colon cancer cells in culture [4] and to exert a remote trophic effect on colonic mucosa [4]
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