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Key metabolomic alterations are associated with ulcerative colitis disease state and activity: a validation analysis
  1. John David Chetwood1,2,
  2. Sudarshan Paramsothy1,2,3,4,
  3. Craig Haifer5,
  4. Thomas J Borody6,
  5. Michael A Kamm7,8,
  6. Rupert W Leong1,2,3,4,
  7. Nadeem O Kaakoush9
  1. 1Department of Gastroenterology, Concord Repatriation General Hospital, Concord, New South Wales, Australia
  2. 2The University of Sydney Faculty of Medicine and Health, Sydney, New South Wales, Australia
  3. 3Department of Gastroenterology, Macquarie University Hospital, Sydney, NSW, Australia
  4. 4Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia
  5. 5Department of Gastroenterology and Hepatology, St Vincent's Hospital, Sydney, New South Wales, Australia
  6. 6Centre for Digestive Diseases, Sydney, New South Wales, Australia
  7. 7Department of Gastroenterology, St Vincent's Hospital, Melbourne, Victoria, Australia
  8. 8Dept of Medicine, University of Melbourne, Melbourne, Victoria, Australia
  9. 9School of Biomedical Sciences, University of New South Wales, Sydney, New South Wales, Australia
  1. Correspondence to Dr John David Chetwood, Department of Gastroenterology, Concord Repatriation General Hospital, Concord, New South Wales 2139, Australia; johnchetwood{at}doctors.org.uk

https://doi.org/10.1136/gutjnl-2023-330196

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    We read with interest the recent paper by Vich Vila et al, which discussed alterations in the metabolome of patients with inflammatory bowel disease (IBD).1 Here, the authors described >300 molecules that were differentially abundant in the faeces of 424 patients with IBD compared with 255 healthy controls, analysed with liquid chromatography with tandem mass spectrometry as well as genome-wide association analysis. Of note, decreased faecal L-urobilin and increased levels of the sphingolipid lactosyl-N-palmitoyl-sphingosine were not only key markers associated with IBD, but furthermore including their ratio improved the accuracy of disease prediction above age, sex, body mass index and faecal calprotectin levels.

    IBD-associated intestinal dysbiosis is characterised by reduced microbial diversity, increases in facultative anaerobes and a decrease in obligately anaerobic producers of short-chain fatty acids, as well as the accumulation of primary unconjugated bile acids and depletion of secondary bile acids.2 The physiological roles of faecal urobilinoids have not been well described, but alterations may be associated with changes in intestinal bacteria capable of their catabolism such as Bacteroides fragilis and Clostridium ramosum (Thomasclavelia ramosa).3 Sphingolipids, produced by the Bacteroidetes phylum, regulate inflammation and immunity via multiple pathways including autophagy, endoplasmic reticulum stress, innate immune responses and G-protein-coupled-receptor signalling.4 Faecal …

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    Footnotes

    • JDC and SP are joint first authors.

    • Twitter @rupertleong, @NOKaakoush

    • JDC and SP contributed equally.

    • Correction notice This article has been corrected since it published Online First. Missing authors, Thomas Borody and Michael Kamm, have now been added and affiliations updated.

    • Contributors JDC: study design, composed the manuscript. NOK, CH, TJB, MK, RWL and SP: data acquisition, data analysis, critical manuscript review.

    • 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 None declared.

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