Impact of disease location on fecal calprotectin levels in Crohn’s disease

Abstract

Objective. The correlation between the Simple Endoscopic Score for Crohn’s Disease (SES-CD) and fecal calprotectin is well established in (ileo)colonic Crohn’s disease (CD). However, for ileal CD, existing data are conflicting. The aim of this study is to evaluate the biomarker profile in CD patients with varying severity and location of mucosal ulceration. Materials and methods. An electronic patient database search identified CD patients in whom ileocolonoscopy, fecal calprotectin (CALPRO), serum C-reactive protein (CRP) and blood leukocyte counts (LEU) were measured within a 4-week interval without changes in medication. Ileocolonoscopies were scored for the presence of ulcers in each segment as defined by the SES-CD and the sum of segmental ulcer scores resulted in a partial SES-CD (pSES-CD). Results. Fourty-four patients were identified, of whom 9/44 had ileal CD, 20/44 colonic and 15/44 ileocolonic CD based on the Montreal classification. In the total study population CALPRO correlated best with pSES-CD (r = 0.76, p < 0.0001), followed by LEU (r = 0.54, p = 0.0004) and CRP (r = 0.45, p = 0.0026). Patients with ileal CD had significantly lower CALPRO level than those with (ileo)colonic disease even in the presence of large and/or very large ulcers (mean ± SEM: 297 ± 81 μg/g vs. 1523 ± 97 μg/g, p < 0.0001). LEU was also significantly lower in the presence of large and/or very large ulcers in ileal CD compared to those with (ileo)colonic disease (mean ± SEM: 6.7 ± 0.9 × 10⁹/l vs. 10.6 ± 0.8 × 10⁹/l, p = 0.02). A similar trend was identified regarding CRP levels. Conclusions. Even in the presence of large or very large ulcers, patients with ileal Crohn’s may not have markedly elevated fecal calprotectin levels.

Key Words:

• Biomarker
• Crohn’s disease
• CRP
• endoscopy
• fecal calprotectin
• SES-CD

Acknowledgement

KG conceived the study, carried out data collection and analysis and drafted the manuscript. JB and SvW performed data collection and helped to draft the manuscript. ML, CP and GvdB consulted the study design and the manuscript in preparation. GD consulted the concept, supervised the design and the manuscript preparation. All authors read and approved the final manuscript. Funding: None declared. Part of this work was presented as an oral presentation at UEGW, Berlin, 2013.

Declaration of interest: K. Gecse has served as speaker for MSD, Abbvie and Ferring Pharmaceuticals. J. Brandse and S. van Wilpe have no conflicts of interest to declare. M. Löwenberg has served as speaker for Abbott, MSD and Ferring. C. Ponsioen has received unrestricted research grants from Abbott Netherlands, Dr. Falk Pharma Benelux, Schering-Plough Netherlands, Tramedico Netherlands and has taken part in advisory boards for Abbott and Glaxo Smith Kline. G. van den Brink has received consulting fees from Abbott laboratories and lecture fees from Abbott Laboratories, Merck Sharp & Dohme and Ferring Pharmaceuticals. He has received research grants from Abbott laboratories and Ferring Pharmaceuticals. G. D’Haens has received consultancy fees from Abbott Laboratories, Actogenix, Centocor, Cosmo, Engene, Ferring Pharmaceuticals, GlaxoSmithKline, Jansen Biologics, Millenium Pharmaceuticals, MSD, Novonordisk, PDL Biopharma, Pfizer, SetPoint, Shire, Sigmoid Pharma Ltd, Takeda, Teva, Tillotts Pharma, UCB; research grants from Abbott Laboratories, Jansen Biologics, Given Imaging, MSD, DrFalk Pharma, Photopill; speaking honoraria from Abbott Laboratories, Jansen Biologics, Tillotts, Tramedico, Ferring, MSD, UCB, Norgine and Shire.