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Increased urinary nitric oxide oxidation products in children with active coeliac disease.

Authors :
van Straaten, EA
Koster-Kamphuis, L
Bovee-Oudenhoven, IM
van der Meer, R
Forget, P-Ph
Source :
Acta Paediatrica; 06/28/99, Vol. 88 Issue 5, 1 Diagram, 1 Chart
Publication Year :
1999

Abstract

Background: Nitric oxide (NO) production catalyzed by iNOS (inducible NO synthase) is thought to take place mainly in macrophages after activation by inflammatory mediators. NO is subsequently oxidized to nitrite and nitrate, which are excreted in urine. The concentration of inflammatory mediators in small bowel biopsy specimens from patients with coeliac disease is increased. The latter could induce increased NO production by stimulation of intestinal macrophage iNOS, resulting in high levels of urinary NO oxidation products, nitrite and nitrate (NOx). Aim: In the present study we evaluated the urinary NOx/creatinine ratios in children with active coeliac disease (n= 22), coeliac disease patients on a gluten-free diet (n= 9), healthy (n= 11) and sick control children (n= 18). Methods: The Griess reagent method was used for measuring urinary NOx. Results: Median NOx/creatinine ratios of active coeliac disease patients, coeliac disease patients on a gluten-free diet, healthy and sick control patients were 1.21, 0.19, 0.10 and 0.13 mmol/mmol, respectively. All active coeliac disease patients showed increased NOx/creatinine ratios. Urinary NOx/creatinine ratios of the active coeliac disease patients were significantly higher than those of healthy controls (p< 0.0001), sick controls (p< 0.0001) and coeliac disease patients on a gluten-free diet (p< 0.0001). Conclusion: The urinary NOx/creatinine ratio is increased in patients with active coeliac disease and reverts to normal on a gluten-free diet. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
08035253
Volume :
88
Issue :
5
Database :
Complementary Index
Journal :
Acta Paediatrica
Publication Type :
Academic Journal
Accession number :
4347416
Full Text :
https://doi.org/10.1111/j.1651-2227.1999.tb00169.x