title: Effects of aspirin and Helicobacter pylori on the gastroduodenal mucosal permeability to sucrose.
abstract: BACKGROUND
  A non-invasive marker is needed to identify patients with significant gastrointestinal injury due to non-steroidal anti-inflammatory drugs. Gastrointestinal permeability to sucrose has been suggested as such a test.
  
  
  OBJECTIVE
  To assess the utility of sucrose permeability as a marker of gastroduodenal mucosal injury after single and multiple doses of aspirin, to identify the site of increased sucrose permeability, to explore the relation between sucrose permeability and endoscopic findings, and to evaluate whether Helicobacter pylori infection influenced gastroduodenal sucrose permeability.
  
  
  METHODS
  After a fasting urine was obtained, 500 ml of a solution containing 100 g of sucrose was ingested. Urine was collected for five hours and assayed for sucrose by high performance liquid chromatography. Sucrose permeability was also assessed 20 minutes after ingestion of 650 mg of aspirin and eight to 12 hours after a 72 hour course of 650 mg aspirin four times a day. The site of increased permeability was identified after pyloric occlusion with a double balloon tube.
  
  
  RESULTS
  Thirty seven healthy volunteers participated. Sucrose permeability (mean (SEM)) increased after both single (195.2 (27) mg and multiple (196.4 (31) mg) doses of aspirin compared with baseline (53.7 (10) mg; p < 0.0005). Balloon pyloric occlusion confirmed that the site of increased sucrose permeability was the stomach. The effect of aspirin on sucrose permeability was similar in those with and without H pylori infection.
  
  
  CONCLUSIONS
  These results confirm the use of sucrose permeability as a marker of aspirin induced gastroduodenal mucosal injury and identify the stomach as the major site of increased permeability. H pylori infection does not seem to change gastric mucosal sucrose permeability either at baseline or after ingestion of aspirin.
authors.affiliation: Department of Medicine, Baylor College of Medicine, Texas, USA.
authors.forename: A A
authors.initials: AA
authors.lastname: Rabassa
authors.forename: R
authors.initials: R
authors.lastname: Goodgame
authors.forename: F M
authors.initials: FM
authors.lastname: Sutton
authors.forename: C N
authors.initials: CN
authors.lastname: Ou
authors.forename: C
authors.initials: C
authors.lastname: Rognerud
authors.forename: D Y
authors.initials: DY
authors.lastname: Graham
mesh_terms: D000328:Adult; D001241:Aspirin / Q000009:adverse effects*; D015415:Biomarkers; D002851:Chromatography, High Pressure Liquid; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects*; D005767:Gastrointestinal Diseases / Q000139:chemically induced* / Q000150:complications; D016481:Helicobacter Infections / Q000150:complications*; D016480:Helicobacter pylori / Q000302:isolation & purification*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011706:Pyloric Antrum / Q000187:drug effects; D013395:Sucrose / Q000494:pharmacology* / Q000652:urine
chemical_list: D015415:Biomarkers; D013395:Sucrose; D001241:Aspirin