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TREM-1, the ideal predictive biomarker for endoscopic healing in anti-TNF-treated Crohn’s disease patients?
  1. Bram Verstockt1,2,
  2. Sare Verstockt3,
  3. Helene Blevi2,
  4. Isabelle Cleynen3,
  5. Magali de Bruyn2,
  6. Gert Van Assche1,2,
  7. Séverine Vermeire1,2,
  8. Marc Ferrante1,2
  1. 1 Department of Gastroenterology and Hepatology, University Hospitals Leuven, KU Leuven, Leuven, Belgium
  2. 2 Department of Chronic Diseases, Metabolism and Ageing, Translational Research Centre for Gastrointestinal Disorders (TARGID-IBD), KU Leuven, Leuven, Belgium
  3. 3 Laboratory for Complex Genetics, Department of Human Genetics, KU Leuven, Leuven, Belgium
  1. Correspondence to Prof Marc Ferrante, Department of Gastroenterology and Hepatology, UZ Leuven, Leuven, B3000, Belgium; marc.ferrante{at}

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We read with great interest the study by Gaujoux et al, who described a whole blood marker for anti-tumour necrosis factor (TNF) responsiveness in patients with Crohn’s disease (CD). The availability of anti-TNF agents dramatically changed therapeutic strategies for patients with CD. However, an overall non-response rate of 30% has been observed, and, together with the approval of new classes of biological agents with a different mode of action, clearly indicates the need for predictive biomarkers. Gaujoux et al identified triggering receptor expressed on myeloid cells 1 (TREM1) expression in whole blood as a biomarker for anti-TNF (non)response (higher expression in responders).1 In inflamed colonic tissue, TREM1 expression is also decreased in future infliximab responders.1 2 TREM-1 is known to amplify inflammation, whereas TREM-1 inhibition in vivo attenuates colitis by modulating autophagy and endoplasmic reticulum (ER) stress.3

We first measured serum TREM-1 (sTREM-1) (Human sTREM-1 ELISA (HK348), Hycult Biotech, Uden, the Netherlands) in 85 patients with CD with active disease prior to anti-TNF therapy (table 1). To reduce the risk of including treatment failures secondary to immunogenicity (and not drug mechanistic failure) or non-drug-related healers, all included patients had to have a good drug exposure, defined as a maintenance trough level >3.0 µg/mL for infliximab or >5.0 µg/mL for adalimumab. Interestingly, patients who achieved mucosal healing (complete absence of ulcerations and erosions4) after 6 months of anti-TNF therapy (adalimumab and infliximab) had significantly lower baseline sTREM-1 levels compared with non-responders (50.8 pg/mL …

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