Our aim was to investigate whether there are changes in permeability to sucrose in asymptomatic Helicobacter pylori gastritis. Nineteen asymptomatic subjects with Helicobacter pylori-associated gastritis with no or mild mucosal atrophy and 19 age- and sex-matched normal controls were studied by peroral load of sucrose (100 g). The fraction of the given oral dose of sucrose excreted in urine was increased in subjects with Helicobacter pylori gastritis (median 0.08% versus 0.04% in controls). Sucrose excretion was not related to atrophy, intestinal metaplasia, or inflammation in the gastric mucosa. However, sucrose permeability was related to the degree of inflammatory (neutrophil) activity, since moderate activity was associated with higher sucrose excretion than mild activity (median 0.13% vs 0.07%). Asymptomatic Helicobacter pylori gastritis was associated with an increased sucrose permeability, which could be a sign of gastric mucosal leakage. This could have implications for the diseases and complications associated with Helicobacter pylori infection.