Fecal calprotectin concentration is increased in children with celiac disease: relation with histopathological findings

Abstract

The aim of this study was to compare the fecal calprotectin concentration in children with newly diagnosed celiac disease, children with celiac disease strictly adhering to a gluten-free diet and healthy controls. We also tried to correlate the fecal calprotectin concentration with the clinical presentation, degree of neutrophilic infiltration and the severity of histopathological injury (Marsh grade) in the small bowel mucosa. The study included three groups: children with untreated celiac disease, children with treated celiac disease, and healthy controls. Moreover, we obtained a second fecal sample from nine newly diagnosed children when their endomysial antibody became negative after gluten-free diet. Fecal calprotectin concentrations were significantly higher in newly diagnosed celiac patients (n=31) compared to patients on gluten-free diet (n=33) and healthy controls (n=34) (117.2 μg/g (3.2-306) vs. 3.7 μg/g (0.5-58.2) and 9.6 μg/g (1-70), respectively, p<0.001). Patients presenting with gastrointestinal symptoms had higher fecal calprotectin concentration compared to the patients presenting with nongastrointestinal symptoms [142.8 (12.2-306) vs. 79.7 (3.2-243.2) respectively, p=0.04]. Nine newly diagnosed patients gave a second fecal sample after starting gluten-free diet when endomysial antibody became negative. Their fecal calprotectin concentration had decreased from 113.7 μg/g (8.7-295.2) to 4.2 μg/g (0.5-20.7) (p<0.01). Increased fecal calprotectin concentration can be used as a non-invasive marker that might aid in the diagnosis of celiac disease, especially in patients with gastrointestinal presentation. Fecal calprotectin concentration returns to normal on a strict gluten-free diet. Fecal calprotectin may be used as a marker of diet adherence and improvement in gastrointestinal inflammation in children with celiac disease. Additionally, it may be used for the differentiation of celiac disease from functional disorders of the gastrointestinal system.