Inflamm Bowel Dis. 2024 Nov 11:izae262. doi: 10.1093/ibd/izae262. Online ahead of print.

Teagan S Edwards ¹, Shaun S C Ho ^1 2 3 4, Stephanie C Brown ¹, Laura Appleton ¹, Briana R Smith ⁵, Grace M Borichevsky ⁵, Akhilesh Swaminathan ⁶, Christopher M A Frampton ⁶, Richard B Gearry ^6 7, Anthony J Kettle ⁵, Andrew S Day ¹

Author information

¹Department of Paediatrics, University of Otago, Christchurch, New Zealand.

²Department of Gastroenterology and Clinical Nutrition, The Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia.

³Department of Paediatrics, University of Melbourne, Melbourne, Victoria, Australia.

⁴Murdoch Children's Research Institute, Melbourne, Victoria, Australia.

⁵Department of Pathology and Biomedical Sciences, Matai Haora-Centre for Redox Biology and Medicine, University of Otago, Christchurch, New Zealand.

⁶Department of Medicine, University of Otago, Christchurch, New Zealand.

⁷Department of Gastroenterology, Christchurch Hospital, Christchurch, New Zealand.

Abstract

Background: Crohn's disease (CD) is a major form of inflammatory bowel disease (IBD) which has relapsing and remitting symptoms. Better ways to detect and monitor active disease are required for early diagnosis and optimal outcomes. We assessed fecal myeloperoxidase (fMPO), a neutrophil-derived enzyme that produces hypochlorous acid, as a marker of disease activity in children with CD.

Methods: This observational study assessed myeloperoxidase (MPO) levels in fecal samples from children aged <17 years with CD (51 with active or 42 inactive disease) measured by enzyme-linked immunosorbent assay (ELISA) and compared to controls (35 healthy siblings and 15 unrelated well children). Results were correlated with fecal calprotectin, serum C-reactive protein, urinary glutathione sulfonamide (a biomarker of hypochlorous acid), and disease activity scores. Differences between groups were assessed by analysis of variance. Receiver-operating-characteristic curves were used to assess how biomarkers predicted disease and disease activity.

Results: Fecal myeloperoxidase activity and fMPO protein correlated with fecal calprotectin (r = 0.78, P < .0001, and r = 0.81, P < .0001, respectively). Fecal myeloperoxidase activity and protein levels were significantly higher (P ≤ .0001) in individuals with active disease compared to healthy sibling controls, unrelated well children, and those with inactive disease. A 9.7 µg/g fMPO protein cutoff distinguished inactive from active disease (sensitivity = 75%, specificity = 76%). Urinary GSA was elevated in children with active disease (P < .0001) and correlated with fMPO protein (r = 0.43, P = .0002) in a subset of 72 children with IBD and controls.

Conclusions: Fecal myeloperoxidase may be superior to fCal at reflecting disease severity in children with CD and produces the damaging oxidant hypochlorous acid during active inflammation.