DECREASE IN GASTRIC PERMEABILITY TO SUCROSE FOLLOWING CURE OF HELICOBACTER-PYLORI INFECTION

Background. Gastric sucrose permeability is a noninvasive marker that reliably increases in association with gastrointestinal injury due to use of nonsteroidal antiinflammatory drugs. Despite the effect of Heli cobacter pylori infection on the gastric mucosa, in a previous study w e were unable to demonstrate that H. pylori infection was associated w ith abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeab ility; therefore, we evaluated the effect of treatment of H. pylori in fection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes. Materials an d Methods. Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was c ollected and assayed for sucrose by high-performance liquid chromatogr aphy. Sucrose permeability was assessed both before and approximately 4 weeks after anti-H. pylori therapy. Results. Seventeen asymptomatic H. pylori-infected volunteers participated; 8 were cured. Sucrose perm eability was in the range commonly found in normal controls both befor e and after anti-H. pylori therapy (mean excretion, 76.3 mg; range, 13 -171 mg). Gastric sucrose permeability correlated with the density of polymorphonulcear cell infiltration of the mucosa. Cure of the H. pylo ri infection was associated with a small but significant decrease in s ucrose permeability (98.8 +/- 18 mg to 51.7 +/- 9.8 mg (p = .01). Sucr ose permeability was greater in those with a high density of mucosal p olymorphonuclear cells compared to those with lower scores (119.5 +/- 4 vs 71.4 +/- 13 for those with scores greater than or equal to 5 comp ared to scores less than or equal to 4; p = .023). Failed therapy resu lted in an increase in the mucosal density of polymorphonuclear infilt ration and sucrose permeability (56.4 +/- 13 mg-99.7 +/- 19 mg pretrea tment vs posttreatment, respectively; p = .031). Conclusion. H. pylori gastritis causes a small but measurable increase in gastric permeabil ity to sucrose that may reflect epithelial transmigration of neutrophi ls.