Relationship of faecal calprotectin and long-term outcomes in Finnish patients with Crohn’s disease: retrospective multi-centre chart review study

Abstract

Background and Aims: A retrospective non-interventional, multi-centre patient chart review study was conducted to investigate the association of faecal calprotectin (FC) 1 year (±2 months) after biological therapy initiation with composite event-free survival (CEFS) consisting of surgical procedures, corticosteroid initiation, treatment failure or dose increase in patients with Crohn’s disease (CD). In addition, the correlations of FC and other tests of disease activity were assessed.

Materials and methods: Data on Finnish CD patients initiating a biological therapy between 2010 and 2016, were collected. The association of FC and CEFS was analysed with Kaplan-Meier and Cox proportional hazard modelling. The correlations were tested with Pearson’s test.

Results: Biological therapy was initiated in 186 patients, of which 87 (46.8%) had FC results available at 1 year and 80 had follow-up exceeding 14 months. The characteristics of patients with and without FC results were similar. Patients with elevated FC (>250 µg/g) had a significantly increased risk of experiencing composite event (HR 3.4, 95% CI: 1.3–8.9; p = .013) when compared to patients with normal FC (FC ≤ 100). No such risk was observed in patients with intermediately increased FC level (100 µg/g < FC ≤ 250 µg/g) (HR 2.2 (95% CI: 0.8–6.2; p = .120). FC value had significant positive correlation with CRP, HBI and leukocyte values when measured at similar timepoints.

Conclusions: Elevated level of FC approximately 1 year after the initiation of biological therapy was associated with an increased risk of either surgical procedures, corticosteroid initiation, treatment failure or dose increase (i.e. composite outcome) in patients with CD.

Keywords:

• Biological treatment
• Crohn’s disease
• faecal calprotectin
• outcomes

Author contributions

Study management (ES, SV, PaMo, TH, VV, RN, DN), conceptualisation (DN, ES, SV, TH, PaMo), design (all), permits (PeMa, PaMo, ES, TH, AJ, CGB, HK, SV); data collection method (PeMa, ES, TH), acquisition (PaMo, AJ, CGB, HK), management (PeMa, TH); analysis design (TH, ES, PaMo, CGB, VV), analysis (TH), interpretation (all); initial manuscript drafting (TH), critical revision and final approval (all).

Disclosure statement

CGB has been in receipt of consulting fees from Abbvie, MSD, Ferring, Takeda, Janssen-Cilag and Pfizer, speaker fees from Abbvie, MSD and Pfizer and travel support from Abbvie, MSD, Ferring and Tillotts Pharma. AJ has been in receipt of speaker fees and travel support from Abbvie, Ferring, Janssen-Cilag, MSD, MEDA, Mylan, Pfizer, Takeda and Tillotts Pharma; consulting fees from Abbvie, Janssen-Cilag, MSD, Pfizer, Takeda and Tillotts Pharma. HK has been in receipt of travel support from MSD and Tillotts Pharma, and consulting fees from Janssen-Cilag. TH, ES and PeMa are employees of ESiOR Oy, the company commissioned by Jansen-Cilag to help perform this study. TH and ES are also shareholders of ESiOR, and ES is the CEO of ESiOR. ESiOR carries out studies, consultancy, education, reporting and health economic evaluations for several pharmaceutical, food industry, diagnostics and device companies, hospitals and academic institutions. Neither TH, ES nor PeMa received any direct financial support as individuals. TH, ES and PeMa declare no personal conflict of interest. SV, VV, DN and RN are employees of Janssen Cilag. SV, VV, DN and RN declare no personal conflict of interests. PaMo has been in receipt of speaker fees and travel support from Abbvie, Ferring, MSD, Janssen-Cilag, and Tillotts Pharma and consulting fees from Abbvie, AOP Orphan Pharmaceuticals, Janssen-Cilag, MSD, Pfizer, Tillotts Pharma, and Takeda.

Additional information

Funding

This work was funded by Janssen-Cilag, Espoo, Finland.