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Fecal calprotectin concentration predicts outcome in inflammatory bowel disease after induction therapy with TNFα blocking agents

Molander, Pauliina MD1,2*; af Björkesten, Clas-Göran MD3; Mustonen, Harri DSc4; Haapamäki, Johanna MD, PhD3; Vauhkonen, Matti MD, PhD6; Kolho, Kaija-Leena MD, PhD5; Färkkilä, Martti MD, PhD2,3; Sipponen, Taina MD, PhD3

doi: 10.1002/ibd.22863
Original Article: Original Clinical Articles

Background: Fecal calprotectin (FC) concentration is a useful surrogate marker for mucosal healing (MH) during tumor necrosis factor alpha (TNFα)-blocking therapy for inflammatory bowel disease (IBD). Our aim was to evaluate whether a normal FC after induction therapy with TNFα antagonist predicts the outcome of IBD patients during maintenance therapy.

Methods: Sixty IBD patients (34 Crohn's disease [CD], 26 ulcerative colitis [UC]), treated with TNFα antagonists, either infliximab (n = 42) or adalimumab (n = 18), and having a documented FC level at baseline and after induction therapy were included. Disease activity was evaluated by partial Mayo score without endoscopy or Harvey–Bradshaw index at baseline, after induction, and at 12 months during maintenance therapy.

Results: After induction, FC was normalized (≤100 μg/g) in 31 patients (52%, median 42 μg/g, range 0–97), whereas the level remained elevated in 29 patients (48%, median 424 μg/g, range 116–5859). At ≈12 months, 26/31 (84%, 18 CD, 8 UC) of the patients with normal FC after induction were in clinical remission, whereas only 11/29 (38%, 9 CD, 2 UC) of those with an elevated (≥100 μg/g) postinduction FC were in clinical remission, P < 0.0001. After induction therapy with TNFα antagonists, a cutoff concentration of 139 μg/g for FC had a sensitivity of 72% and a specificity of 80% to predict a risk of clinically active disease after 1 year.

Conclusions: A normal FC after induction therapy with TNFα antagonists predicts sustained clinical remission in the majority of patients on scheduled therapy with active luminal disease. (Inflamm Bowel Dis 2012;)

1 Maria Helsinki City Hospital and University of Helsinki, Helsinki, Finland

2 University of Helsinki, Helsinki, Finland

3 Department of Medicine, Division of Gastroenterology, Helsinki University Central Hospital, Helsinki, Finland

4 Helsinki University Central Hospital, Department of Surgery, Biomedicum Helsinki, Finland

5 Department of Medicine, Division of Gastroenterology, Helsinki University Central Hospital, Jorvi Hospital, Espoo, Finland

6 Children's Hospital, Helsinki University Central Hospital, Helsinki, Finland

* Department of Medicine, Division of Gastroenterology, Maria Helsinki City Hospital, P.O.B. 6501, Helsinki, Finland FIN-00099

Email: pauliina.molander@welho.com

Received 19 October 2011; Accepted 29 November 2011

Published online 4 January 2012 in Wiley Online Library (wileyonlinelibrary.com).

fn4 Supported by a grant from the Helsinki University Central Hospital Research Fund (EVO-grant), a grant from the Finnish Cultural Foundation, a grant from the Mary and George C. Ehrnrooth Foundation, and a grant from the Finnish Foundation for Gastroenterological Research.

© Crohn's & Colitis Foundation of America, Inc.
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