Background: The gastric mucosal alcohol dehydrogenase activity was reported to be reduced in subjects with Helicobacter pylori-associated chronic gastritis. However, the role of H. pylori infection in the metabolism of ingested ethanol has not been fully elucidated. Aim: To clarify whether H. pylori infection exerts any influence on the metabolism of small amounts of ethanol in humans. Subjects and methods: 13C-ethanol (100 μL) diluted in 100 mL water was administered orally to 22 healthy volunteers before breakfast. Breath samples were then collected every 10 min for up to 60 min. The content of 13CO2 (‰) was analysed using a mass-spectrometric method. The excretion rate of labelled CO2 was analysed by calculation of the following mathematical parameters, i.e., T max, Cmax, and AUC60. Results: In H. pylori-negative controls (n = 11), the Tmax, Cmax and AUC60 were 0.47 ± 0.13, 19.1 ± 6.0 and 13.7 ± 4.5, respectively. The corresponding values were 0.53 ± 0.16 (n.s.) and 12.7 ± 4.8 (P < 0.05) and 9.0 ± 3.6 (P < 0.05), respectively, in subjects with H. pylori infection (n = 11). Successful eradication of H. pylori was associated with significant increase of these parameters (Cmax and AUC60, n = 6). Conclusions: The metabolism of small amounts of ethanol is attenuated in subjects with H. pylori infection.
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