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Atrophic gastritis is associated with increased sucrose permeability related to chronic inflammation
Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of clinical chemistry.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Neuroscience and Locomotion, Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
Linköping University, Faculty of Health Sciences. Linköping University, Department of Biomedicine and Surgery, Division of surgery. Östergötlands Läns Landsting, Centre of Surgery and Oncology, Department of Surgery in Östergötland.
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2005 (English)In: Digestion, ISSN 0012-2823, E-ISSN 1421-9867, Vol. 72, no 4, 201-206 p.Article in journal (Refereed) Published
Abstract [en]

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. Conclusion: 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. Copyright © 2005 S. Karger AG.

Place, publisher, year, edition, pages
2005. Vol. 72, no 4, 201-206 p.
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Medical and Health Sciences
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URN: urn:nbn:se:liu:diva-31495DOI: 10.1159/000089145Local ID: 17290OAI: oai:DiVA.org:liu-31495DiVA: diva2:252318
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2017-12-13

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Sjöstedt, CamillaHannestad, UlfFranzén, LennartSöderholm, Johan DBorch, Kurt

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Sjöstedt, CamillaHannestad, UlfFranzén, LennartSöderholm, Johan DBorch, Kurt
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Faculty of Health SciencesDivision of surgeryDepartment of Surgery in ÖstergötlandDivision of clinical chemistryPathologyDepartment of Clinical Pathology and Clinical Genetics
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