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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, …
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.
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