Journal of pediatric gastroenterology and nutrition · 1997
Sucrose permeability in children with gastric damage and Helicobacter pylori infection.
Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Vera J F, Gotteland M, Chavez E, Vial M T, Kakarieka E, Brunser O
Аннотация
BACKGROUND: Increased permeability to sucrose has been recently shown to be a good marker of gastric mucosal damage in adults.
METHODS: This test was evaluated in 40 children consulting for recurrent abdominal pain and the results were correlated with endoscopic and histologic findings and with the presence of H. pylori.
RESULTS: The gastric mucosa was considered endoscopically normal in 31 children; 3 had duodenitis and 6 had mild gastritis. Abnormal endoscopic findings were associated with increased urinary sucrose excretion (MANOVA F = 7.30; p = 0.002). In the 6 children with mild gastritis, mean sucrose excretion was twice that of controls (0.060 +/- 0.024 vs. 0.029 +/- 0.018, respectively; p = 0.019) and significantly higher than the group with duodenitis (0.037 +/- 0.013; p = 0.038). The specificity and sensitivity of sucrose permeability test for detection of gastric damage were 90.3% and 83.3%, respectively. H. pylori was detected in 62.5% of children including all patients with mild gastritis, in 2 out of 3 with duodenitis and 17 out of 31 endoscopically normal controls. No differences in sucrose excretion were observed in relation with the presence of H. pylori or histological findings in the control group.
CONCLUSIONS: Urinary sucrose excretion is a good marker of mucosal gastric damage in children and may be used as a screening test in large groups of populations.
METHODS: This test was evaluated in 40 children consulting for recurrent abdominal pain and the results were correlated with endoscopic and histologic findings and with the presence of H. pylori.
RESULTS: The gastric mucosa was considered endoscopically normal in 31 children; 3 had duodenitis and 6 had mild gastritis. Abnormal endoscopic findings were associated with increased urinary sucrose excretion (MANOVA F = 7.30; p = 0.002). In the 6 children with mild gastritis, mean sucrose excretion was twice that of controls (0.060 +/- 0.024 vs. 0.029 +/- 0.018, respectively; p = 0.019) and significantly higher than the group with duodenitis (0.037 +/- 0.013; p = 0.038). The specificity and sensitivity of sucrose permeability test for detection of gastric damage were 90.3% and 83.3%, respectively. H. pylori was detected in 62.5% of children including all patients with mild gastritis, in 2 out of 3 with duodenitis and 17 out of 31 endoscopically normal controls. No differences in sucrose excretion were observed in relation with the presence of H. pylori or histological findings in the control group.
CONCLUSIONS: Urinary sucrose excretion is a good marker of mucosal gastric damage in children and may be used as a screening test in large groups of populations.