Published online May 21, 2019. doi: 10.3748/wjg.v25.i19.2354
Peer-review started: March 7, 2019
First decision: April 11, 2019
Revised: April 16, 2019
Accepted: April 19, 2019
Article in press: April 20, 2019
Published online: May 21, 2019
Crohn’s disease (CD) is a chronic and disabling disorder that can highly affect quality of life. Faecal calprotectin (Fcal) is a well-accepted monitoring tool and a surrogate marker of mucosal healing and could then be an alternative to endoscopy. Recently, the CALM trial compared two ways of monitoring patients with inflammatory bowel disease (IBD) treated with adalimumab. The authors reported that the group monitored using a tight control of inflammation with objective markers of disease activity and clinical symptoms to drive treatment decisions, achieved better endoscopic and clinical outcomes than conventional monitoring. In a post-hoc analysis of this study, the authors reported that most of the therapeutic intensification were related to increased level of Fcal in the tight control group. However, even though the conclusion of this landmark trial encourages IBD physicians to use Fcal testing in daily practice, the authors did not explore specifically the value of each marker, i.e., CD activity index (CDAI), C-reactive protein (CRP) and Fcal.
Understanding the value of each monitoring biomarker to guide physicians to manage patients with inflammatory bowel disease is a key point.
In this study, we aimed to investigate the performances of CDAI, CRP and Fcal variation, alone or combined, after 12 wk of anti-tumor necrosis factor (TNF) therapy to predict corticosteroids-free remission (CFREM) at one year, in CD patients treated with anti-TNF.
It was a multicentre prospective observational study.
Among the 40 included patients, 13 patients (32.5%) achieved CFREM at W52. In univariable analysis, CDAI < 150 at W12 (P = 0.012), CRP level < 2.9 mg/L at W12 (P = 0.001) and Fcal improvement at W12 [Fcal < 300 μg/g; or, for patients with initial Fcal < 300 μg/g, at least 50% decrease of Fcal or normalization of Fcal (<100 μg/g)] (P = 0.001) were predictive of CFREM at W52. Combined endpoint (CDAI < 150 and CRP ≤ 2.9 mg/L and FCal improvement) at W12 was the best predictor of CFREM at W52 with PPV = 100.0% (100.0-100.0) and NPV = 87.1% (75.3-98.9). In multivariable analysis, Fcal improvement at W12 [odd ratio (OR) = 45.1 (2.96-687.9); P = 0.03] was a better predictor of CFREM at W52 than CDAI < 150 [OR = 9.3 (0.36-237.1); P = 0.145] and CRP < 2.9 mg/L (0.77-278.0; P = 0.073).
The combined monitoring of CDAI, CRP and FCal after anti-TNF induction therapy is able to predict favorable outcome within one year in patients with CD. The most impactful biomarker was Fcal among these three biomarkers. Our results should lead IBD physicians to monitor patients with CD using a tight control strategy based on CDAI, CRP and Fcal in daily practice.
Additional studies from independent cohorts should be conducted to confirm these data.