Helicobacter pylori but not gastrin is associated with the development of colonic neoplasms |
| |
| Authors: | Michael Selgrad Jan Bornschein Arne Kandulski Carla Hille Jochen Weigt Albert Roessner Thomas Wex Peter Malfertheiner |
| |
| Affiliation: | 1. Department of Gastroenterology Hepatology and Infectious Diseases, Otto‐von‐Guericke‐University of Magdeburg, , Magdeburg, Germany;2. Department of Pathology, Otto‐von‐Guericke‐University of Magdeburg, , Magdeburg, Germany;3. Medical Laboratory for Clinical Chemistry, Microbiology and Infectious Diseases, Department of Molecular Genetics, , Magdeburg, Germany |
| |
| Abstract: | Recent studies have suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of colonic neoplasia. Hypergastrinemia can be induced by H. pylori infection, and gastrin can act as putative promoter of colorectal carcinogenesis. Aim of our study was to assess whether H. pylori infection and/or increased serum gastrin levels are associated with the occurrence of colonic neoplasms. For this, we reviewed prospectively collected data of 377 patients with a minimum age of 50 years who underwent colonoscopy. H. pylori and CagA status were determined by serology. Serum gastrin levels were measured in fasting state by commercially available assay. In H. pylori infected patients (n = 138; 36.6%), the overall prevalence of colonic neoplasms was more frequent compared to H. pylori negative patients (n = 239; 63.4%) (OR = 2.73, 95% CI: 1.76–4.24). H. pylori infection occurred more frequently in patients with hyperplastic polyps (OR = 2.66, 95% CI: 1.23–5.74) and adenomas presenting with low grade intraepithelial neoplasia (IEN) (OR = 1.85, 95% CI: 1.14–2.99). Attributable risk for adenomas with high grade IEN and colorectal adenocarcinoma (n = 14) was not assessed due to the low number of cases. The expression of CagA was also associated with an increased risk for colonic neoplasms (OR = 2.25, 95% CI: 1.29–3.94). Hypergastrinemia did not increase the risk for any colonic neoplasms and there was no difference in basal serum gastrin levels between H. pylori positive and negative patients. In conclusion, H. pylori infection, including CagA expression is associated with an increased risk for the development of colonic neoplasm. |
| |
| Keywords: | Helicobacter pylori gastrin colonic neoplasms |
|
|
