Fecal Calprotectin Concentration in Celiac Disease

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dc.contributor.authorErtekin, Vildan
dc.contributor.authorSelimoglu, Mukadder Ayse
dc.contributor.authorTurgut, Ahmet
dc.contributor.authorBakan, Nuri
dc.date.accessioned2024-08-04T20:32:31Z
dc.date.available2024-08-04T20:32:31Z
dc.date.issued2010
dc.departmentİnönü Üniversitesien_US
dc.description.abstractGoals: We aimed to determine fecal calprotectin (FC) concentration and its relation with histopathologic findings of children with celiac disease (CD) and to observe the probable alterations under gluten-free diet (GFD). Background: As FC is regarded as a marker of inflammation in the gastrointestinal tract, we hypothesized that it might be increased in untreated CD. Study: The study included 29 newly diagnosed patients with CD (mean age: 6.6 +/- 0.6 y) and sex and age-matched 10 healthy children. All of the children with CD admitted to the hospital were classical form who has chronic diarrhea and failure to thrive. The degree of mucosal damage was graded according to the modified Marsh criteria. FC concentration was determined by enzyme-linked immunosorbent assay method on admission and after 1 year of GFD. Results: Mean FC concentration of children with CD on admission and of healthy children were 13.40 +/- 8.5 and 4.3 +/- 3.3 mg/L, respectively (P = 0.004). FC concentration under GFD was 4.6 +/- 2.7 mg/L and there was a significant statistical difference between untreated patients and those under GFD for 1 year (P = 0.001). There was no statistical difference between FC concentration of those under GFD and healthy children (P = 0.8). Mean FC concentrations of children with total-villous atrophy and partial-villous atrophy were significantly different (13.8 +/- 9.3 mg/L vs. 3.7 +/- 1.8 mg/L, P = 0.005). Conclusions: It was found that FC concentration is increased in childhood CD, related to the severity of histopathologic findings and responsive to GFD. The pathogenetic mechanism by which FC is increased in CD should be investigated in further studies.en_US
dc.identifier.doi10.1097/MCG.0b013e3181cadbco
dc.identifier.endpage546en_US
dc.identifier.issn0192-0790
dc.identifier.issue8en_US
dc.identifier.pmid20054281en_US
dc.identifier.scopus2-s2.0-77955931612en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage544en_US
dc.identifier.urihttps://doi.org/10.1097/MCG.0b013e3181cadbco
dc.identifier.urihttps://hdl.handle.net/11616/95110
dc.identifier.volume44en_US
dc.identifier.wosWOS:000281115300006en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.relation.ispartofJournal of Clinical Gastroenterologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectceliac diseaseen_US
dc.subjectfecal calprotectinen_US
dc.subjectchildrenen_US
dc.titleFecal Calprotectin Concentration in Celiac Diseaseen_US
dc.typeArticleen_US

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