Journal Summary: Do Antibiotics Predispose to the Development of Inflammatory Bowel Disease?

Brief Overview of the Study

Imbalances in the gut microbiota, also known as dysbiosis, can be caused by external factors such as antibiotics, leading to a decrease in the diversity of gut flora. Such imbalances can predispose individuals to inflammatory bowel disease (IBD), and this association has been reported in current pediatric literature. Research has shown that the use of antibiotics during childhood, and even during the peripartum period, can lead to the development of IBD in the future.[1] [2]

There is, however, a limited data available on the relation between antibiotic use and the risk of developing IBD in adults. To address this, a population-based cohort study was conducted by Faye et al. They utilized data from Danish nationwide registries and followed up on over 6 million individuals aged 10 years and above for a period of 18 years (2000–2018). The study was aimed to assess the impact of the dose–response relationship, timing, and class of antibiotics on the risk of developing IBD.[3] Since the study was done with the help of the Danish Civil Registration System, which carefully maintains patient data and prescriptions list, the risk of recall and selection bias and loss to follow-up were eliminated. The study found that antibiotic exposure was associated with an increased risk of IBD for all age groups, with the incidence risk ratio (IRR) being greatest among individuals aged 40 to 60 and ≥ 60 years (age 10–40 years, IRR 1.28, 95% confidence interval [CI] 1.25–1.32; age 40–60 years, IRR 1.48, 95% CI 1.43–1.54; age ≥ 60 years, IRR 1.47, 95% CI 1.42–1.53). For all age groups a positive dose–response was observed for both ulcerative colitis (UC) and Crohn's disease (CD). The study also found that the highest risk of developing IBD was observed 1 to 2 years after exposure to antibiotics, the risk increasing with number of courses (IRRs per antibiotic course were 1.11 [95% CI 1.10–1.12], 1.15 [95% CI 1.14–1.16], and 1.14 [95% CI 1.13–1.15] for individuals aged 10–40, 40–60, and ≥ 60 years). Most cases were reported after the use of antibiotic classes that are commonly prescribed to treat gastrointestinal (GI) pathogens, such as nitroimidazoles or fluoroquinolones. However, some cases were reported after the use of other non-GI-related antibiotics, such as narrow-spectrum penicillin. Interestingly, there was no association between IBD and nitrofurantoin, which is used to treat urinary tract infections and does not extensively affect the GI tract. This finding supports the hypothesis that dysbiosis in the gut can lead to IBD.

Ethical Statement

None.

Authors' Contributions

P.P. wrote the initial draft, performed the search, and reviewed the literature. A.C. reviewed the manuscript critically. Both approved the manuscript.

Data Availability Statements

There is no data associated with this work.

Publication History

Received: 14 May 2024

Accepted: 03 June 2024

Article published online:
29 July 2024

• References

• 1 Azad MB, Konya T, Persaud RR. et al; CHILD Study Investigators. Impact of maternal intrapartum antibiotics, method of birth and breastfeeding on gut microbiota during the first year of life: a prospective cohort study. BJOG 2016; 123 (06) 983-993
• 2 Hviid A, Svanström H, Frisch M. Antibiotic use and inflammatory bowel diseases in childhood. Gut 2011; 60 (01) 49-54
• 3 Faye AS, Allin KH, Iversen AT. et al. Antibiotic use as a risk factor for inflammatory bowel disease across the ages: a population-based cohort study. Gut 2023; 72 (04) 663-670
• 4 Kaplan GG. The global burden of IBD: from 2015 to 2025. Nat Rev Gastroenterol Hepatol 2015; 12 (12) 720-727
• 5 Kaplan GG, Windsor JW. The four epidemiological stages in the global evolution of inflammatory bowel disease. Nat Rev Gastroenterol Hepatol 2021; 18 (01) 56-66
• 6 Ianiro G, Tilg H, Gasbarrini A. Antibiotics as deep modulators of gut microbiota: between good and evil. Gut 2016; 65: 1906-1915
• 7 Frank DN, St Amand AL, Feldman RA, Boedeker EC, Harpaz N, Pace NR. Molecular-phylogenetic characterization of microbial community imbalances in human inflammatory bowel diseases. Proc Natl Acad Sci U S A 2007; 104 (34) 13780-13785
• 8 Walker AW, Sanderson JD, Churcher C. et al. High-throughput clone library analysis of the mucosa-associated microbiota reveals dysbiosis and differences between inflamed and non-inflamed regions of the intestine in inflammatory bowel disease. BMC Microbiol 2011; 11: 7
• 9 Yadav A, Yadav R, Sharma V, Dutta U. A comprehensive guide to assess gut mycobiome and its role in pathogenesis and treatment of inflammatory bowel disease. Indian J Gastroenterol 2024; 43 (01) 112-128
• 10 Jha DK, Mishra S, Dutta U, Sharma V. Antibiotics for inflammatory bowel disease: current status. Indian J Gastroenterol 2024; 43 (01) 145-159
• 11 Cross E, Saunders B, Farmer AD, Prior JA. Diagnostic delay in adult inflammatory bowel disease: a systematic review. Indian J Gastroenterol 2023; 42 (01) 40-52
• 12 Ng SC, Tang W, Leong RW. et al; Asia-Pacific Crohn's and Colitis Epidemiology Study ACCESS Group. Environmental risk factors in inflammatory bowel disease: a population-based case-control study in Asia-Pacific. Gut 2015; 64 (07) 1063-1071
• 13 Diallo D, Somboro AM, Diabate S. et al. Antituberculosis therapy and gut microbiota: review of potential host microbiota directed-therapies. Front Cell Infect Microbiol 2021; 11: 673100
• 14 Ponziani FR, Zocco MA, D'Aversa F, Pompili M, Gasbarrini A. Eubiotic properties of rifaximin: disruption of the traditional concepts in gut microbiota modulation. World J Gastroenterol 2017; 23 (25) 4491-4499
• 15 Kondamudi PK, Malayandi R, Eaga C, Aggarwal D. Drugs as causative agents and therapeutic agents in inflammatory bowel disease. Acta Pharm Sin B 2013; 3 (05) 289-296
• 16 Hou JK, Abraham B, El-Serag H. Dietary intake and risk of developing inflammatory bowel disease: a systematic review of the literature. Am J Gastroenterol 2011; 106 (04) 563-573
• 17 Zeng MY, Inohara N, Nuñez G. Mechanisms of inflammation-driven bacterial dysbiosis in the gut. Mucosal Immunol 2017; 10 (01) 18-26