Exclusive enteral nutrition (EEN) has been recommended as the first-line therapy in children with active Crohn disease (CD). The primary aim of our study was to determine whether it is possible to use the difference between basal fecal calprotectin (F-CPT) and the value at week 2 of EEN to predict clinical response at week 6. We prospectively collected stool samples for F-CPT analysis and clinical and laboratory parameters during EEN from 38 pediatric patients (28 boys, median age 12.8 years) with newly diagnosed active luminal CD. The difference between F-CPT concentrations before EEN and at week 2 did not predict clinical non-response at week 6 (OR 0.9996 95% CI 0.9989-1.0002, p = 0.18); however, it predicted patients who did not achieve clinical remission at week 6 (OR 0.9993, 95% CI 00.9985-0.9998, p = 0.006) with sensitivity of 58%, and specificity of 92% for cut-off of F-CPT increase by 486 μg/g.Conclusions: An early decrease in F-CPT levels in children with newly diagnosed active luminal CD did not predict clinical response at week 6 of EEN induction therapy, and clinical remission was predicted with low accuracy. Therefore, F-CPT cannot be used as a predictor to select the patients in whom EEN should be terminated. What is Known: • The fecal calprotectin (F-CPT) is an important marker of intestinal inflammation. • Approximately 25% of pediatric patients with Crohn disease (CD) do not achieve clinical remission, and there is still no sufficient predictor of response to exclusive enteral nutrition (EEN) treatment. What is New: • The difference between the F-CPT concentrations before EEN treatment and at week 2 did not predict clinical response to treatment at week 6, even if it predicted clinical remission, however, with low accuracy. F-CPT is not a suitable predictor to select the patients for discontinuing of EEN induction therapy.

Department of Pediatrics University Hospital Motol and 2nd Faculty of Medicine Charles University Prague 5 Uvalu 84 150 06 Prague 5 Czech Republic

Eur J Pediatr. 2018 Nov;177(11):1695. doi: 10.1007/s00431-018-3260-5. PubMed

Zobrazit více v PubMed

Clin Lab. 2014;60(12):1993-2000 PubMed

J Gastroenterol Hepatol. 2006 Oct;21(10):1609-14 PubMed

Clin Gastroenterol Hepatol. 2006 Jun;4(6):744-53 PubMed

J Pediatr Gastroenterol Nutr. 2011 Jan;52(1):38-42 PubMed

J Clin Gastroenterol. 2011 Mar;45(3):234-9 PubMed

Aliment Pharmacol Ther. 2014 Jun;39(12):1398-407 PubMed

Aliment Pharmacol Ther. 2007 Sep 15;26(6):795-806 PubMed

World J Gastroenterol. 2014 Mar 28;20(12):3191-7 PubMed

World J Gastroenterol. 2011 Dec 21;17(47):5166-71 PubMed

Dig Liver Dis. 2006 Jun;38(6):381-7 PubMed

Gut. 2015 Mar;64(3):438-46 PubMed

Gut. 2000 Oct;47(4):506-13 PubMed

Scand J Gastroenterol. 2014 Apr;49(4):434-41 PubMed

J Crohns Colitis. 2015 Jan;9(1):26-32 PubMed

J Pediatr Gastroenterol Nutr. 2014 Jun;58(6):795-806 PubMed

Inflamm Bowel Dis. 2012 Jan;18(1):55-62 PubMed

Clin Gastroenterol Hepatol. 2008 Nov;6(11):1218-24 PubMed

J Crohns Colitis. 2014 Oct;8(10):1179-207 PubMed

J Crohns Colitis. 2010 Feb;4(1):7-27 PubMed

Aliment Pharmacol Ther. 2011 Jun;33(12):1332-9 PubMed

Inflamm Bowel Dis. 2012 Sep;18(9):1672-81 PubMed

Inflamm Bowel Dis. 2006 Jun;12(6):524-34 PubMed

Aliment Pharmacol Ther. 2008 Feb 15;27(4):293-307 PubMed

Dig Dis Sci. 2016 Jul;61(7):2041-50 PubMed

Inflamm Bowel Dis. 2007 Sep;13(9):1100-5 PubMed

J Gastroenterol. 2014 Apr;49(4):638-45 PubMed

J Pediatr Gastroenterol Nutr. 2004 Mar;38(3):270-5 PubMed

Aliment Pharmacol Ther. 2009 Sep 1;30(5):501-7 PubMed

Aliment Pharmacol Ther. 2008 Nov 15;28(10):1221-9 PubMed

Int J Colorectal Dis. 2007 Apr;22(4):429-37 PubMed