Upper Gastrointestinal Disease Influences the Occurrence of Inflammatory Bowel Disease

Sonnenberg A1, Turner KO2, Genta RM2,3. Dig Dis Sci. 2019 Nov 27. doi: 10.1007/s10620-019-05972-1. [Epub ahead of print]


Author information

Division of Gastroenterology, Portland VA Medical Center, P3-GI, Oregon Health & Science University, Portland, OR, 97239, USA. sonnenbe@ohsu.edu.

Inform Diagnostics, Irving, TX, USA.

Baylor College of Medicine, Houston, TX, USA.


BACKGROUND AND AIMS: Compromise of the gastric acid barrier may facilitate bacterial invasion of the lower intestinal tract and influence the occurrence of inflammatory bowel disease (IBD). Our study tested the associations between histopathologic changes in the upper and lower gastrointestinal tract in patients undergoing bidirectional endoscopy.

METHODS: The Inform Diagnostics database is a national electronic repository of histopathologic records of patients distributed throughout the entire USA. A case-control study among 302,061 patients, of whom 13,943 harbored IBD, evaluated whether the occurrence of Crohn's disease or ulcerative colitis was influenced by the presence of various upper gastrointestinal diagnoses associated with lowered gastric acid output. The influence of individual risk factors on the occurrence of colonic disease was expressed as odds ratios with their 95% confidence intervals.

RESULTS: The odds ratio for Crohn's disease being associated with gastric H. pylori was 0.30 (0.24-0.37), with intestinal metaplasia 0.30 (0.24-0.39), with fundic gland polyps 0.42 (0.35-0.50), with gastric hyperplastic polyps 0.35 (0.23-0.51), with Barrett's metaplasia 0.19 (0.14-0.24), and with reflux esophagitis 0.46 (0.42-0.51). The odds ratio for ulcerative colitis being associated with gastric H. pylori was 0.58 (0.50-0.67), with intestinal metaplasia 0.39 (0.32-0.47), with fundic gland polyps 0.61 (0.53-0.71), with gastric hyperplastic polyps 0.64 (0.49-0.84), with Barrett's metaplasia 0.50 (0.43-0.59), and with reflux esophagitis 0.77 (0.71-0.84).

CONCLUSIONS: A diminished gastric acid barrier function, as evidenced by various upper gastrointestinal diseases associated with lowered gastric acid output, may exert a protective influence against the development of inflammatory bowel disease.

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