Helicobacter pylori infection and lactose intolerance increase expiratory hydrogen

Wolfgang J Schnedl; Nathalie Meier-Allard; Michael Schenk; Sonja Lackner; Dietmar Enko; Harald Mangge; Sandra J Holasek

doi:10.17179/excli2021-4508

Helicobacter pylori infection and lactose intolerance increase expiratory hydrogen

EXCLI J. 2022 Feb 17:21:426-435. doi: 10.17179/excli2021-4508. eCollection 2022.

Authors

Wolfgang J Schnedl¹, Nathalie Meier-Allard², Michael Schenk³, Sonja Lackner², Dietmar Enko⁴, Harald Mangge⁴, Sandra J Holasek²

Affiliations

¹ Practice for General Internal Medicine, Dr. Theodor Körnerstrasse 19b, A-8600 Bruck/Mur, Austria.
² Division of Immunology and Pathophysiology, Otto Loewi Research Center, Medical University of Graz, Heinrichstrasse 31a, A-8010 Graz, Austria.
³ Das Kinderwunsch Institut Schenk GmbH, Am Sendergrund 11, A-8143 Dobl, Austria.
⁴ Clinical Institute of Medical and Chemical Laboratory Diagnosis, Medical University of Graz, Auenbruggerplatz 30, A-8036 Graz, Austria.

Abstract

Infection with Helicobacter pylori (H.pylori) may cause dyspepsia and/or unexplained functional nonspecific, gastrointestinal complaints of the irritable bowel syndrome (IBS) spectrum. Hitherto, in H. pylori infected patients with symptoms of the IBS spectrum the occurrence of additional food intolerance/malabsorption is not evaluated. We used a retrospective analysis of charts from 548 patients who presented with gastrointestinal complaints of the irritable bowel syndrome spectrum. An enzyme-linked IgA immunosorbent assay or histologic evaluation of gastric mucosa were used to detect H. pylori infection. A hydrogen breath (H₂) test was performed to evaluate fructose malabsorption (FM) and lactose intolerance (LIT). Serum diamine oxidase value of <10 U/ml and a response to a histamine-reduced diet was used to identify histamine intolerance (HIT). We found 293 patients infected with H. pylori, within these were 58 H. pylori patients with LIT, 23 H. pylori LIT patients with FM and 46 H. pylori LIT patients with HIT. Additionally, 13 H. pylori, lactose- and histamine intolerance patients also had FM. The Kruskal Wallis test and pairwise comparison were used to analyze differences of the area under the curve of expiratory hydrogen. In lactose H₂ breath tests compared with LIT-only patients, LIT with H. pylori, LIT and H. pylori with HIT, LIT and H. pylori with FM showed significantly higher exhaled H₂ levels (p=0.022). Pairwise comparison demonstrated H. pylori infected patients with LIT exhaled more H₂ compared to LIT-only (p=0.029). H. pylori with lactose- and histamine intolerance, and H. pylori with lactose-, histamine intolerance and FM compared to H. pylori-only patients indicated a significantly higher occurrence of stomach pain during lactose H₂ breath tests (p=0.012 and p=0.005, respectively). We demonstrate that LIT patients with high expiratory H₂ levels in lactose breath tests may have H. pylori infection and possibly additional food intolerance/malabsorption. Subsequently, besides H. pylori eradication, a dietician is necessary for an individually tailored reduction- or exclusion diet of symptom triggering food components.

Keywords: diamine oxidase; fructose malabsorption; histamine intolerance; irritable bowel syndrome; lactose intolerance.