Exhaled Hydrogen after Lactulose Hydrogen Breath Test in Patient with Duodenal Ulcer Disease—A Pilot Study for Helicobacter-pylori-Associated Gastroduodenal Disease

Abstract

Objectives: The precipitating mechanism(s) from the inactive to the active stage of duodenal ulcer disease (DU) is unclear. It has been shown that hydrogen gas from colonic fermentation provides an important energy source for Helicobacter pylori (Hp) colonization. The lactulose hydrogen breath test (LHBT) is a useful tool to assess the small intestinal and/or colon fermentation. This study examines the association(s) between the status of gastroduodenal disease and the result of a lactulose hydrogen breath test (LHBT). Materials and Methods: We enrolled Hp-positive active duodenal ulcer (aDU) patients, inactive DU (iDU) patients and patients with a positive Hp infection without structural gastroduodenal lesion, i.e., simple gastritis (SG Hp+). The patients with simple gastritis without Hp infection (SG Hp-) served as controls. Histological examinations of the gastric mucosa and lactulose hydrogen breath test (LHBT) were performed. Results: SG Hp + patients tend to have advanced gastritis (pangastritis or corpus-predominant gastritis) compared with SG Hp-patients (7/29 vs. 0/14, p = 0.08). More iDU patients had advanced gastritis than either the SG Hp + (7/9 vs. 7/29, p = 0.006) or aDU patients (7/9 vs. 6/24, p = 0.013). In comparison with the aDU patients, the iDU patients were also older (52.1 ± 12.6 vs. 42.2 ± 11.9 years, p = 0.02) and had a lower mean area under the curve value of the LHBT(AUC) (209.1 ± 86.0 vs. 421.9 ± 70.9, p = 0.023). Conclusion: aDU patients with a positive Hp infection have a lower grade of gastric mucosa damage than iDU patients and tend to have a higher level of exhaled hydrogen after LHBT.

Protease XIV abolishes NHE inhibition by empagliflozin in cardiac cells

“…Inhibition of SGLT2 leads to glycosuria, resulting in the excretion of 40–75 g of glucose per day in diabetic or prediabetic patients ( Veelen et al, 2023 ). Apart from their SGLT2-dependent effects on the kidney, including modulating of substrate metabolism, fluid balance, and hemodynamics, SGLT2i has been found to have direct effects on various cell types largely lacking SGLT2, such as cardiomyocytes, endothelial cells, platelets and fibroblast ( Chen et al, 2022 ; Dyck et al, 2022 ). These effects also involve myocardial infarction and ischemia-reperfusion (I/R) ( Andreadou et al, 2017 ).…”