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  • Faecal calprotectin is a surrogate marker of biliary inflammation in primary sclerosing cholangitis associated inflammatory bowel disease

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Liver
Original research
Faecal calprotectin is a surrogate marker of biliary inflammation in primary sclerosing cholangitis associated inflammatory bowel disease
  1. Polychronis Pavlidis1,2,
  2. Deepak Joshi2,3,
  3. Yasser El Sherif2,3,
  4. Ben Warner2,3,
  5. Shraddha Gulati2,
  6. James Alexander4,
  7. Gemma Cross5,
  8. Tracy Dew5,
  9. Hadil Abu Arqoub6,
  10. John Devlin2,3,
  11. Michael Heneghan3,
  12. Patrick Dubois2,
  13. Ingvar Bjarnason7,
  14. Nick Powell4,
  15. Bu'Hussain Hayee2
  1. 1 Experimental Immunobiology, King's College London, London, UK
  2. 2 King's Institute of Therapeutic Endoscopy, King's College Hospital, London, UK
  3. 3 Institute of Liver Studies, King's College Hospital, London, UK
  4. 4 Imperial College London Faculty of Medicine, London, UK
  5. 5 Biomarker Discovery, Viapath, King's College Hospital, London, UK
  6. 6 Pathology Department, Viapath, King’s College Hospital, London, Algeria
  7. 7 Department of Gastroenterology, King's College Hospital, London, UK
  1. Correspondence to Dr Polychronis Pavlidis, King's College London, London WC2R 2LS, UK; polychronis.pavlidis{at}kcl.ac.uk; Dr Nick Powell; nicholas.powell{at}imperial.ac.uk

Abstract

Objective Faecal calprotectin (fCAL) is an established marker of intestinal inflammation in inflammatory bowel disease (IBD). Disproportionally high fCAL levels, for the severity of intestinal inflammation, have been previously observed in primary sclerosing cholangitis associated IBD (PSC-IBD). The aim of this study was to test the hypothesis that fCAL is a marker of biliary injury in PSC-IBD.

Methods We used two cohorts: (1) post hoc analysis of a colonoscopic surveillance study allowing correlation of fCAL to endoscopic severity as measured by the ulcerative colitis endoscopic index of severity (UCEIS) in PSC-IBD (n=20) and ulcerative colitis (UC, n=20) and (2) prospective recruitment of patients attending for endoscopic retrograde cholangiopancreatography allowed the correlation of fCAL to biliary calprotectin (n=8).

Results A strong correlation was seen between fCAL and UCEIS in UC (r=0.821, 95% CI (0.585 to 0.929), p<0.0001). In PSC-IBD, the correlation was weaker (r=0.596, 95% CI (0.195 to 0.8260), p=0.006). PSC-IBD patients with endoscopically quiescent colitis (UCEIS: 0–1) had higher fCAL than patients with UC (279 µg/g, IQR (68–601) vs 30 µg/g, IQR (14–107), p=0.015) . This was associated with higher risk of biliary complications like need for antibiotics or instrumentation (HR 16.39, 95% CI (2.98 to 90.25)) rather than colitis flares (follow-up: 12 months). Calprotectin measured in faeces correlated positively with biliary calprotectin (r=0.898, p=0.0024).

Conclusion fCAL is a surrogate marker for biliary inflammation in PSC-IBD.

Trial registration number NCT02543021.

  • PRIMARY SCLEROSING CHOLANGITIS
  • IBD

Data availability statement

Data are available on reasonable request. Not applicable.

https://doi.org/10.1136/flgastro-2021-102053

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    Data availability statement

    Data are available on reasonable request. Not applicable.

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    Footnotes

    • NP and B'HH are joint senior authors.

    • Twitter @thebiledoc@djosh78, @IBDdoc

    • Contributors PP conceived the study, collected, analysed and interpreted data, wrote the manuscript, YES, BW, SG, JA, JD and PD recruited patients, performed procedures, collected samples, contributed to manuscript preparation. GC, TD and HAA performed calprotectin testing and immunohistochemistry, contributed to manuscript preparation, MAH and IB contributed to manuscript preparation, NP and B'HH provided financial support, supervision and contributed to manuscript preparation. PP acts as guarantor of the study.

    • Funding Polychronis Pavlidis has been supported with a PhD studentship by the King’s Medical Research Trust.

    • Competing interests None declared.

    • Provenance and peer review Not commissioned; externally peer reviewed.