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Fecal Calprotectin Concentration in Celiac Disease

Ertekin, Vildan MD*; Selimoğlu, Mukadder Ayşe MD; Turgut, Ahmet MD*; Bakan, Nuri MD

Journal of Clinical Gastroenterology: September 2010 - Volume 44 - Issue 8 - pp 544-546
doi: 10.1097/MCG.0b013e3181cadbc0
Original Article

Goals: 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.

*Faculty of Medicine, Division of Pediatric Gastroenterology, Department of Hepatology and Nutrition, Ataturk University

Department of Biochemistry, Ataturk University, Erzurum

Faculty of Medicine, Division of Pediatric Gastroenterology, Department of Hepatology and Nutrition, Inonu University, Malatya, Turkey

The authors declare that they have no conflict of interest regarding the publication of this article.The authors declare that they have no funding declaration.

Reprints: Vildan Ertekin, MD, Faculty of Medicine, Department of Pediatric Gastroenterology, Hepatology and Nutrition, Ataturk University, Tip Fakultesi, Cocuk Sagligi ve Hastaliklari AD, 25240 Erzurum, Turkey (e-mail: vildanertekin@hotmail.com).

Received for publication June 4, 2009; accepted November 11, 2009

© 2010 Lippincott Williams & Wilkins, Inc.