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Mendelian randomization study of inflammatory bowel disease and type 1 diabetes.

Authors :
Zhu JY
Ma X
Liu MY
Ma LZ
Sun XR
Yan MY
Xue C
Sun C
Source :
Endocrine [Endocrine] 2024 Dec; Vol. 86 (3), pp. 943-953. Date of Electronic Publication: 2024 Jul 31.
Publication Year :
2024

Abstract

Purpose: Our purpose was to investigate and test the causal relationship between type 1 diabetes (T1D) and inflammatory bowel disease (IBD) and its major phenotypes, including ulcerative colitis (UC) and Crohn's disease (CD), in two large datasets.<br />Methods: We obtained IBD samples from the largest publicly available genome-wide association study (GWAS), as well as the FinnGen database and the publicly accessible IEU GWAS database of T1D. We employed a two-sample Mendelian randomization approach to assess bidirectional causality using the inverse variance weighting (IVW) method as the primary outcome.<br />Results: Genetic predisposition to T1D was associated with reduced risk of IBD (IVW: odds ratio (OR), 0.867; 95% confidence interval (CI), [0.852, 0.883]; P < 0.001), UC (OR = 0.879 [0.823, 0.939], P < 0.001), and CD (OR = 0.925 [0.872, 0.981], P = 0.009). The republication results found IBD genetically possessed negative association with T1D (OR = 0.781 [0.684, 0.891], P < 0.001). Additionally, a meta-analysis of results was conducted to prove the strong evidence between T1D and CD (OR = 0.95 [0.91, 0.98]; p = 0.01).<br />Conclusions: This study first demonstrated a causal effect of TID on the reduced risk of CD in the mendelian randomization study.<br />Competing Interests: Compliance with ethical standards Ethics approval and Consent to participate No ethical approval from an ethics committee or Equator Network checklist was necessary as our study did not involve any human or animal research or observational studies. Our investigation utilized Mendelian randomization analysis and draw data from open databases. All of the projects and datasets cited in our study were approved by the respective ethics committees of the corresponding published articles. Conflict of interest The authors declare no competing interests.<br /> (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Details

Language :
English
ISSN :
1559-0100
Volume :
86
Issue :
3
Database :
MEDLINE
Journal :
Endocrine
Publication Type :
Academic Journal
Accession number :
39083171
Full Text :
https://doi.org/10.1007/s12020-024-03919-9