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We read with interest the randomised controlled trial by Dierikx et al that demonstrated the lack of long-term impact of antenatal antibiotics on offspring gut microbiome.1 Antibiotics in early life are implicated in IBD risk, potentially mediated by gut microbiome perturbations and altered host–microbe interactions.2 3 However, data on offspring IBD risk with maternal antibiotics exposure during pregnancy are limited and conflicting.4 5 We conducted a population-based cohort study to better understand this relationship, including the impact of cumulative antibiotic exposure, the trimester of antibiotic exposure and narrow-spectrum versus broad-spectrum antibiotics on offspring IBD risk.
Using historical, prospectively collected data in cross-linked nationwide Danish registers of individuals born between 1997 and 2003 and followed up to 2018, we estimated the impact of systemic antibiotic exposure during pregnancy on offspring risk of IBD, Crohn’s disease (CD) and UC after adjusting for relevant covariates. Further details are available in online supplemental materials.
A total of 416 833 (8 103 366 person-years) pregnant women-offspring dyads were included of whom 296 974 (71.2%), 80 036 (19.2%), 25 335 (6.1%) and 14 488 (3.5%) received 0, 1, 2 and ≥3 courses of antibiotics, respectively. Mothers with immune-mediated diseases and smoking during pregnancy received antibiotics more frequently than those …
Twitter @manasiagrawalmd, @KristineAllin, @PREDICTIBD
Contributors MA: study concept and design, interpretation of data, drafting and critical revision of the manuscript for important intellectual content; GP: study design, acquisition, analysis and interpretation of data, critical revision of the manuscript for important intellectual content; J-FC: interpretation of data and critical revision of the manuscript for important intellectual content; KHA: study concept and design, interpretation of data and critical revision of the manuscript for important intellectual content; TJ: study concept and design, interpretation of data and critical revision of the manuscript for important intellectual content.
Funding This study was funded by the Danish National Research Foundation (grant number DNRF148). MA is supported by the National Institute of Diabetes and Digestive and Kidney Diseases (K23DK129762-01). J-FC is supported by the Mount Sinai (New York) SUCCESS fund (grant number N/A).
Competing interests MA reports no conflict of interest. GP reports no conflict of interest. J-FC reports receiving research grants from AbbVie, Janssen Pharmaceuticals and Takeda; receiving payment for lectures from AbbVie, Amgen, Allergan, Ferring Pharmaceuticals, Shire and Takeda; receiving consulting fees from AbbVie, Amgen, Arena Pharmaceuticals, Boehringer Ingelheim, Bristol Myers Squibb, Celgene Corporation, Eli Lilly, Ferring Pharmaceuticals, Galmed Research, Glaxo Smith Kline, Geneva, Iterative Scopes, Janssen Pharmaceuticals, Kaleido Biosciences, Landos, Otsuka, Pfizer, Prometheus, Sanofi, Takeda and TiGenix; and hold stock options in Intestinal Biotech Development. KHA reports no conflict of interest. TJ reports no conflict of interest.
Provenance and peer review Not commissioned; externally 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.
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