title: Atrophic gastritis is associated with increased sucrose permeability related to chronic inflammation.
abstract: BACKGROUND
  Different theories have been presented to explain how atrophic gastritis may lead to gastric cancer development. One contributing factor could be impaired function of the gastric mucosal barrier. The aim of this study was to investigate if there are changes in gastric mucosal permeability to sucrose in atrophic gastritis.
  
  
  METHODS
  The study comprised 22 patients with atrophic gastritis and 21 normal controls. Gastritis was classified according to the Sydney system from endoscopic biopsies of the gastric corpus and antrum. All subjects were exposed to oral sucrose load (100 g), and the fraction of sucrose excreted in urine was measured by gas chromatography-mass spectrometry.
  
  
  RESULTS
  The fraction of sucrose excreted in urine after oral load was significantly increased in atrophic gastritis compared with controls (median 0.08 vs. 0.04%; p = 0.003). Sucrose excretion was positively related to the degree of chronic inflammation (median fraction excreted: mild inflammation 0.06%, moderate inflammation 0.08%, severe inflammation 0.18%; p = 0.04) rather than to the degree of atrophy in the gastric mucosa. Occurrence of intestinal metaplasia was also associated with significantly higher sucrose excretion. However, in multivariate analysis, including intestinal metaplasia, only the degree of inflammation was positively related to sucrose excretion.
  
  
  CONCLUSIONS
  Atrophic gastritis is associated with increased sucrose permeability, suggesting paracellular leakage of the gastric mucosa. This leakage seems to be related to the degree of inflammation rather than the degree of atrophy. The findings may have implications for the diseases and complications associated with atrophic gastritis.
authors.affiliation: Department of Biomedicine and Surgery, University Hospital of Linköping, Sweden.
authors.forename: Camilla
authors.initials: C
authors.lastname: Sjöstedt Zsigmond
authors.forename: Ulf
authors.initials: U
authors.lastname: Hannestad
authors.forename: Lennart
authors.initials: L
authors.lastname: Franzén
authors.forename: Johan D
authors.initials: JD
authors.lastname: Söderholm
authors.forename: Kurt
authors.initials: K
authors.lastname: Borch
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002463:Cell Membrane Permeability / Q000502:physiology*; D018450:Disease Progression; D005260:Female; D008401:Gas Chromatography-Mass Spectrometry; D005753:Gastric Mucosa / Q000378:metabolism* / Q000473:pathology; D005757:Gastritis, Atrophic / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008297:Male; D008679:Metaplasia / Q000473:pathology; D008875:Middle Aged; D011379:Prognosis; D013395:Sucrose / Q000493:pharmacokinetics*; D013549:Sweetening Agents / Q000493:pharmacokinetics*
chemical_list: D013549:Sweetening Agents; D013395:Sucrose