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Going deeper: molecular inflammatory scores in IBD
  1. James C Lee1,2
  1. 1Genetic Mechanisms of Disease Laboratory, The Francis Crick Institute, London, UK
  2. 2Institute of Liver and Digestive Health, Royal Free Hospital, University College London, London, UK
  1. Correspondence to Dr James C Lee, Genetic Mechanisms of Disease Laboratory, The Francis Crick Institute, London, London, UK; James.lee{at}

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The management of IBD is evolving. Not long ago, symptomatic relief, or ‘clinical remission’ was the major treatment goal—if not the only goal—for most patients. However, the disconnect between inflammation and symptoms has been long recognised, and there is now abundant evidence that patients with silent inflammation, unsurprisingly, develop more disease-related complications than those with inactive disease.1 For this reason, current IBD management usually involves a ‘treat-to-target’ approach—a concept borrowed from rheumatology2—where objective measures of inflammation are used to ensure that treatment leads to resolution of inflammation as well as of symptoms.3

For such an approach to be effective, however, there is a need for sensitive markers of inflammation that could be used to determine whether or not a therapy is working. Recent years have seen this bar serially raised—with many now advocating for a move from normalised faecal inflammatory markers4 and mucosal healing5 to deeper levels of remission, including histological and transmural healing.6 7 In Gut, Argmann, et al describe the development and validation of two complementary transcriptional scores8—one derived from intestinal biopsies (b/iMIS) and the other from peripheral blood (cirMIS). While exploratory, these raise the prospect of extending disease activity measures into the molecular realm (table 1).

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Table 1

Methods for confirming disease remission in …

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  • Contributors This invited commentary was conceived and written by JCL.

  • Funding JCL is a Lister Institute Prize Fellow and is supported by the Francis Crick Institute which receives its core funding from the UK Medical Research Council (CC2219), Cancer Research UK (CC2219) and the Wellcome Trust (CC2219). For the purpose of Open Access, the author has applied a CC BY public copyright licence to any author accepted manuscript version arising from this submission.

  • Competing interests JCL reports financial support for research from GSK and consultancy fees from Abbvie, AgPlus Diagnostics, PredictImmune and C4X Discovery.

  • Provenance and peer review Commissioned; internally peer reviewed.

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