Helicobacter pylori is a Risk Factor for Colonic Neoplasms

1] Portland VA Medical Center, Portland, Oregon, USA [2] Oregon Health and Science University, Portland, Oregon, USA.
The American Journal of Gastroenterology (Impact Factor: 10.76). 12/2012; 108(2). DOI: 10.1038/ajg.2012.407
Source: PubMed


It has been suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of adenomatous polyps and adenocarcinoma of the colon. Our aim was to study the association between H. pylori-positive gastritis and the occurrence of any colonic neoplasm.

From a computerized database of surgical pathology reports, we selected 156,000 subjects who underwent colonoscopy and esophago-gastro-duodenoscopy with biopsy results from both procedures.

Compared with normal gastric mucosa, H. pylori gastritis occurred more frequently among patients with hyperplastic polyps (OR=1.24, 95% CI: 1.18-1.30), adenomatous polyps (1.52, 1.46-1.57), advanced adenomas (1.80, 1.69-1.92), villous adenomas or adenomas with high-grade dysplasia (1.97, 1.82-2.14), and adenocarcinomas (2.35, 1.98-2.80). Similarly, the strength of the association between H. pylori-positive gastritis and colonic neoplasm increased with size and number of the adenomas. The association between H. pylori gastritis and the occurrence of colonic neoplasm was similar for different locations of the large bowel. Other gastric conditions etiologically associated with H. pylori, such as intestinal metaplasia, adenoma, lymphoma, and adenocarcinoma, were also significantly associated with an increased risk of colonic neoplasm.

Various forms of gastritis related to H. pylori infection confer an increased risk for colonic neoplasm. In the past, when H. pylori infection was more prevalent, its attributable risk to the occurrence of colorectal neoplasm may have been quite substantial.

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Available from: Robert M Genta, Jan 01, 2015
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    • "Despite these limitations, we believe that our study provides meaningful results to the existing literature. To our knowledge, our study has a sample size second only to the study done by Sonnenberg and Genta [11]. Most importantly, we are able to provide insight about the effect of triple therapy, chronic PPI use, and the combination of both in the risk of adenomatous polyp formation. "
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    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.
    Gastroenterology Research and Practice 06/2015; 2015:1-5. DOI:10.1155/2015/638547 · 1.75 Impact Factor
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    • "Therefore, they were not extracted for the performance of this study. In the recent past, this database has been utilized for a large variety of histo-epidemiologic studies [13] [14] [15] [16] [17] [18]. For the purpose of the present study, the database was searched for all records of patients who underwent an esophagogastro-duodenoscopy (EGD) between January 1, 2008 and August 17, 2013. "
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    ABSTRACT: The aim of the study was to utilize a large national histopathology database for the analysis of the clinical epidemiology of gastric polyps. In a case-control study, 71,575 case subjects with gastric polyps were compared to 741,351 control subjects without gastric polyps. Of all patients, 7.72% harboured fundic gland polyps, 1.79% gastric hyperplastic polyps, 0.09% gastric adenomas, and 0.06% type I neuroendocrine tumours. All types showed a clear-cut age-dependent rise. Reflux disease was significantly more common in patients with fundic gland polyps and significantly less common in patients with gastric adenomas or neuroendocrine tumours. Anaemia was more common in patients with gastric hyperplastic polyps, gastric adenomas, or neuroendocrine tumours. Helicobacter pylori was found significantly less frequently in all subjects with gastric polyps than in controls. Intestinal metaplasia and gastric atrophy were both more common in gastric adenoma and neuroendocrine tumours and less common in fundic gland polyps than in controls. Different polyp types tended to coincide in the same patients. Gastric hyperplastic polyps appeared to mark the beginning of a progression from chronic gastritis to intestinal metaplasia and gastric atrophy, which leads to diminished gastric acid output and increased gastrin secretion. Gastric adenoma and neuroendocrine tumours reflect later stages of this process. Copyright © 2014. Published by Elsevier Ltd.
    Digestive and Liver Disease 11/2014; 47(2). DOI:10.1016/j.dld.2014.10.004 · 2.96 Impact Factor
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    • "Changes in nucleotide sequence, single nucleotide polymorphism (SNP), such an insulin growth factor 1 (IGF1) could have an impact on developing CRC and is a high risk for colorectal polyps (Feik et al., 2010). More recent studies have shown another risk factor, H. pylori infection, confers an increased risk for colonic neoplasm (Sonnenberg et al., 2012). For race factors, the Chinese had a higher incidence of CRC than Malaysian but developed colorectal cancer at a later age in Brunei Darussalam (Chong et al., 2009). "
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    ABSTRACT: Background: Colorectal cancer (CRC) is a major cause of morbidity and mortality in the western world and also ranks as the fifth-leading malignancy and death in Thailand. This study aimed to provide a present outlook of colorectal diseases among Thai patients with special emphasis on CRC in Hatyai, Songkhla, southern Thailand. Materials and methods: This retrospective study covered ten year data of CRC, benign colorectal tumors and non-colorectal tumors from the Department of Pathology in Hatyai Hospital, Songkhla, Thailand, between years 2003-2012. Incidence rates based on age, gender, ten year incidence trends, and distribution of histopathological characteristics of patients were calculated and demonstrated. Results: Out of 730 biopsies, 100 cases were benign colorectal tumors, 336 were CRC and 294 were non-colorectal tumors. Colorectal tumors (both benign and CRC) (60.1%) were more common than non-colorectal tumors (39.9%). CRC (77.1%) were more common than benign colorectal tumors (32.9%). Colorectal tumors were mainly found in patients aged over sixty whereas non-colorectal and benign colorectal tumors were found in those under sixty (P=0.01). sAmong CRC, adenocarcinoma contributed about 97.3% of all cases with well differentiated tumors being the most frequent (56.9%). Both benign colorectal tumors and CRC were more commonly found in males (63%) than females (37%). The incidence trend of CRC demonstrated increase from 2003-2012. Conclusions: The incidence of CRC increased in Hatyai from 2003-2012. CRC tends to be more common in people older than sixty, thus, screening programs, cost-effective analysis of treatment modalities, and treatment protocols for the elderly should be examined. Proper implementation of preventive measures such as changing lifestyle factors might enhance control of colorectal disease.
    Asian Pacific journal of cancer prevention: APJCP 04/2013; 14(4):2667-2671. DOI:10.7314/APJCP.2013.14.4.2667 · 2.51 Impact Factor
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