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It is in the matrix: a molecular clue to fibro-stenotic Crohn’s disease
  1. Timon E Adolph
  1. Internal Medicine I, Medizinische Universitat Innsbruck, Innsbruck, Austria
  1. Correspondence to Dr Timon E Adolph, Internal Medicine I, Medizinische Universitat Innsbruck, Innsbruck, Austria; timon-erik.adolph{at}

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Stricturing Crohn’s disease (CD), a consequence of fibrosis occurring during chronic unresolved gut inflammation, is a common problem in clinical praxis for which we currently lack targeted medical therapy.1 Patients typically present with obstructive bowel symptoms and radiographic signs of a stricture that is commonly (but not exclusively) located in the terminal ileum or at the ileocecal valve.2 Histopathology of the stricture reveals CD features, such as submucosal fibrosis by excess extracellular matrix deposition, fibromuscular hyperplasia, chronic transmural inflammation and epithelioid granulomas that are often associated with creeping fat in the resection specimen.3 Creeping fat is partially driven by translocation of mucosal-associated gut bacteria,4 and fibronectin-mediated communication by muscle cells of the nearby bowel wall.5 Moreover, several mediators such as transforming growth factor β, and the family of interleukin 1 (IL-1), IL-6 and IL-36 cytokines promote gut fibrosis, while for example interferon γ acts anti-fibrotic.1

The current mainstay of therapy for CD strictures is endoscopic balloon dilatation or surgical therapy (stricturoplasty or resection), a decision that is based on the discussion with a surgeon and guided by the length and number of strictures, the severity of clinical symptoms, the mucosal presentation and the presence of other …

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  • Contributors none.

  • Funding TA is supported by the European Research Council (ERC-STG: 101039320) and the FWF (FG15).

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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