title: Decrease in gastric permeability to sucrose following cure of Helicobacter pylori infection.
abstract: 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 Helicobacter pylori infection on the gastric mucosa, in a previous study we were unable to demonstrate that H. pylori infection was associated with abnormal gastric sucrose permeability. Our goal in this study was to explore further whether H. pylori infection changed gastric permeability; therefore, we evaluated the effect of treatment of H. pylori infection on gastric permeability to sucrose and the relation of sucrose permeability to density of polymorphonuclear leukocytes.
  
  
  METHODS
  Five hundred milliliters of a solution containing 100 gm of sucrose was ingested by the subject at bedtime. Overnight urine was collected and assayed for sucrose by high-performance liquid chromatography. 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 permeability was in the range commonly found in normal controls both before 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. pylori infection was associated with a small but significant decrease in sucrose permeability (98.8 +/- 18 mg to 51.7 +/- 9.8 mg (p = .01). Sucrose permeability was greater in those with a high density of mucosal polymorphonuclear cells compared to those with lower scores (119.5 +/- 4 vs 71.4 +/- 13 for those with scores > or = 5 compared to scores < or = 4; p = .023). Failed therapy resulted in an increase in the mucosal density of polymorphonuclear infiltration and sucrose permeability (56.4 +/- 13 mg-99.7 +/- 19 mg pretreatment vs posttreatment, respectively; p = .031).
  
  
  CONCLUSIONS
  H. pylori gastritis causes a small but measurable increase in gastric permeability to sucrose that may reflect epithelial transmigration of neutrophils.
authors.affiliation: Department of Medicine, Veterans Affairs Medical Center, Houston, TX 77030, USA.
authors.forename: R W
authors.initials: RW
authors.lastname: Goodgame
authors.forename: H M
authors.initials: HM
authors.lastname: Malaty
authors.forename: H M
authors.initials: HM
authors.lastname: el-Zimaity
authors.forename: D Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D000900:Anti-Bacterial Agents / Q000009:adverse effects / Q000627:therapeutic use; D001692:Biological Transport / Q000187:drug effects; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D008297:Male; D013395:Sucrose / Q000378:metabolism*
chemical_list: D000900:Anti-Bacterial Agents; D013395:Sucrose