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. 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.

Effects of aspirin on gastroduodenal permeability in alcoholics and controls

“…Subsequently, several studies showed that abnormal gastroduodenal permeability to sucrose is a reasonable marker for the presence of gastroduodenal injury in NSAID users (DeMeo, 1995; Erlacher et al, 1998; Meddings et al, 1995; Smecuol et al, 2001; Sutherland et al, 1994). Other researchers used sucrose permeability tests to assess damage to the gastroduodenal mucosa induced by oral corticosteroids (Kiziltas et al, 1998), intense exercise (Lambert et al, 2007b; Pals et al, 1997; Smetanka et al, 1999), Helicobacter pylori infection (Borch et al, 1998; Goodgame et al, 1997), atrophic gastritis (Sjostedt Zsigmond et al, 2005), Crohn’s disease (Wyatt et al, 1997), celiac disease (Smecuol et al, 1997; Vogelsang et al, 1996), coffee (Cibickova et al, 2004), smoking (Gotteland et al, 2002) or a combination of these damaging factors (Gotteland et al, 2002; Lambert et al, 2007a; Lambert et al, 2001; Rabassa et al, 1996; Ryan et al, 1996; Santucci et al, 1995). …”

Unrecognized hypoglycemia due to maltodextrin interference with bedside glucometry

“…Sucrose, a disaccharide of glucose and fructose, is not absorbed through the mucosa of an intact GI tract, but may be absorbed in the presence of barrier breakdown, such as ulcers, inflammation and atrophic gastritis [10,11]. It is presumed that as with sucrose, maltodextrin-or a smaller oligosaccharide metabolite or maltose-may be absorbed by passive diffusion in the setting of gastric inflammation.…”