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Steroid use and misuse: a key performance indicator in the management of IBD
  1. Jonathan Blackwell1,2,
  2. Christian Selinger3,4,
  3. Tim Raine5,
  4. Gareth Parkes6,
  5. Melissa A Smith7,8,
  6. Richard Pollok1,9
  1. 1Department of Gastroenterology, St George's Hospitals NHS Foundation Trust, London, UK
  2. 2School of Public Health, Imperial College London, London, UK
  3. 3Leeds Gastroenterology Institute, Leeds Teaching Hospitals NHS Trust, Leeds, UK
  4. 4The Leeds Institute of Research at St James’, University of Leeds, Leeds, UK
  5. 5Department of Gastroenterology, Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK
  6. 6Department of Gastroenterology, Royal London Hospital, London, UK
  7. 7Digestives Diseases Centre, Brighton and Sussex University Hospitals NHS Trust, Brighton, UK
  8. 8Department of Gastroenterology, Brighton and Sussex Medical School, Brighton, UK
  9. 9Division of Infection and Immunity, St George’s University London, London, UK
  1. Correspondence to Dr Richard Pollok, Division of Infection and Immunity, St George’s University London, London SW17 0RE, UK; rpollok{at}sgul.ac.uk

Abstract

Corticosteroids remain an important tool for inducing remission in inflammatory bowel disease (IBD) but they have no role in maintenance of remission. The significant adverse side effect profile of these drugs means their use should be avoided where possible or measures taken to reduce their risk. Despite an expanding array of alternative therapies, corticosteroid dependency and excess remain common. Appropriate steroid use is now regarded a key performance indicator in the management of IBD. This article aims to outline indications for corticosteroid use in IBD, their risks and strategies to reduce their use and misuse.

  • steroid-sparing efficacy
  • inflammatory bowel disease
  • ulcerative colitis
  • crohn's disease
  • 5-aminosalicylic acid (5-ASA)
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Footnotes

  • Contributors JB wrote the manuscript. All coauthors contributed to editing, preparing and revising the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests JB is supported by a grant provided by Crohn's and Colitis UK (grant number: SP2018/3). CS has received unrestricted research grants from Warner Chilcott, Janssen and AbbVie, has provided consultancy to Warner Chilcott, Falk, AbbVie, Takeda, Fresenius Kabi and Janssen, and had speaker arrangements with Warner Chilcott, Falk, AbbVie, MSD, Pfizer and Takeda. TR has received research/educational grants and/or speaker/consultation fees from Abbvie, BMS, Celgene, Ferring, Gilead, GSK, LabGenius, Janssen, Mylan, MSD, Novartis, Pfizer, Sandoz, Takeda and UCB GCP has received unrestricted grants from AbbVie and Takeda, has provided consultancy for AbbVie, Ferring, Takeda, Napp Pharmaceuticals, Janssen and Tillotts and has speaker arrangements with Ferring, Takeda, Janssen, AbbVie and Falk. RP is supported by funding from Wellcome Trust Institute Strategic Support Fund (ISSF) and Crohn's and Colitis UK grant. He has provided consultancy/ or speakers fees for Napp Pharmaceuticals and Falk. He has had educational grants from Pharmacosmos, Abbvie, Janssen, Warner-Chilcottand Takeda.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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