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Letter
Gut microbial metabolism of 5-aminosalicylic acid in inflammatory bowel disease
  1. Naomi Karmi1,
  2. Shiqiang Sun1,
  3. Eleonora A M Festen1,
  4. Arnau Vich Vila1,2,3,
  5. Ranko Gacesa1,4,
  6. Rinse K Weersma1
  1. 1 Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  2. 2 Department of Microbiology and Immunology, Rega Institute for Medical Research, Leuven, Belgium
  3. 3 Center for Microbiology, VIB-KU Leuven, Leuven, Belgium
  4. 4 Department of Genetics, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
  1. Correspondence to Prof Dr Rinse K Weersma, Department of Gastroenterology and Hepatology, University Medical Centre Groningen, Groningen, The Netherlands; r.k.weersma{at}umcg.nl

https://doi.org/10.1136/gutjnl-2024-332205

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    The effect of the gut microbiome on the bioavailability and efficacy of orally administered drugs is of considerable importance for personalised medicine.1 We, therefore, read with great interest the ‘GI highlights from the literature’ focussing on gut microbial metabolism of 5-aminosalicylic acid (5-ASA) in inflammatory bowel disease (IBD), originally published in the journal Nature Medicine.2 3 Mehta et al. used metagenomics, metatranscriptomics and metabolomics from the IBD-Integrative Human Microbiome Project (HMP2) to identify 12 microbial acetyltransferase gene families that encode 5-ASA inactivating enzymes and confirmed the results using in vitro analyses. They confirmed that four of these genes—profiled in metagenomic data from stool samples—are associated with 5-ASA treatment failure in two cohorts of patients with IBD, implying that it might be possible to predict 5-ASA treatment outcome by profiling gut microbiota of patients. However, to generalise these findings, they need to be confirmed in independent cohorts, preferably from diverse (geographical) backgrounds.

    We, therefore, analysed the presence of these gene families in gut microbiota of the Dutch 1000IBD cohort and their association to 5-ASA treatment failure.4 5 We included 72 patients after excluding participants with a stoma or ileoanal pouch, steroid use within one month before sampling or concomitant drug use during sampling (sulfasalazine, thiopurines, …

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    Footnotes

    • NK and SS are joint first authors.

    • Contributors EAMF, AVV, RG and RKW designed and coordinated the study. NK collected clinical metadata, and EAMF supervised. AVV processed the data. NK, SS, AVV and RG contributed to the data analysis. NK and SS drafted the manuscript. EAMF, AVV, RG and RKW critically reviewed the manuscript. All authors approved 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 NK, SS and AVV declare no conflicts of interest. EAMF has received a research grant from Takeda Pharmaceuticals and is supported by a ZonMW Clinical Fellowship grant (project number 90719075). RG received funding by Janssen Pharmaceuticals (for unrelated research projects), received consulting funding from Esox Biologics (for unrelated research projects). RKW has received unrestricted Research Grants from Takeda, Johnson & Johnson, Ferring and Tramedico and speakers fees from Abbvie, MSD and Boston Scientific and has acted as a consultant for Takeda Pharmaceuticals.

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

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.