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Associations between gastric histopathology and the occurrence of colonic polyps
Author(s) -
Sonnenberg A.,
Turner K. O.,
Genta R. M.
Publication year - 2020
Publication title -
colorectal disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.029
H-Index - 89
eISSN - 1463-1318
pISSN - 1462-8910
DOI - 10.1111/codi.14968
Subject(s) - hyperplastic polyp , medicine , gastroenterology , intestinal metaplasia , odds ratio , gastric polyp , helicobacter pylori , histopathology , stomach , metaplasia , pathology , cancer , colorectal cancer , colonoscopy
Abstract Aim Compromise of the gastric acid barrier may facilitate bacterial invasion of the lower intestinal tract and promote the development of colonic neoplasia. Our study aimed to test the associations between histopathological abnormalities of the upper and lower gastrointestinal tract in patients undergoing bidirectional endoscopy. Method The Inform Diagnostics database is a national electronic repository of histopathological records of patients distributed throughout the USA. A case–control study of 302 061 patients, 163 168 of whom had colonic polyps, evaluated whether the occurrence of colonic polyps was influenced by the presence of the following gastro‐oesophageal diagnoses: gastric Helicobacter pylori infection, gastric intestinal metaplasia, fundic gland polyps and gastric hyperplastic polyps. The influence of individual diagnoses on the occurrence of colonic polyps was expressed as odds ratios with their 95% confidence intervals. Results The odds ratio for tubular adenomas being associated with gastric H. pylori was 1.53 (1.49–1.58), with intestinal metaplasia 1.65 (1.59–1.71), with fundic gland polyps 1.49 (1.45–1.54) and with gastric hyperplastic polyps 1.85 (1.75–1.96). The odds ratio for sessile serrated polyps being associated with gastric H. pylori was 1.03 (0.96–1.10), with intestinal metaplasia 1.21 (1.13–1.30), with fundic gland polyps 1.79 (1.69–1.89) and with gastric hyperplastic polyps 1.52 (1.35–1.71. Conclusion A diminished gastric acid barrier function, which occurs in various upper gastrointestinal diseases associated with lowered gastric acid output, may promote the development of colonic neoplasia.