Our aim was to investigate whether there arechanges in permeability to sucrose in asymptomaticHelicobacter pylori gastritis. Nineteen asymptomaticsubjects with Helicobacter pylori associated gastritis with no or mild mucosal atrophy and 19 age- andsex-matched normal controls were studied by peroral loadof sucrose (100 g). The fraction of the given oral doseof sucrose excreted in urine was increased in subjects with Helicobacter pylori gastritis(median 0.08% versus 0.04% in controls). Sucroseexcretion was not related to atrophy, intestinalmetaplasia, or inflammation in the gastric mucosa.However, sucrose permeability was related to the degreeof inflammatory (neutrophil) activity, since moderateactivity was associated with higher sucrose excretionthan mild activity (median 0.13% vs 0.07% ).Asymptomatic Helicobacter pylori gastritis was associatedwith an increased sucrose permeability, which could bea sign of gastric mucosal leakage. This could haveimplications for the diseases and complicationsassociated with Helicobacter pylori infection.