Graves Disease and Inflammatory Bowel Disease: A Bidirectional Mendelian Randomization
Authors' conclusion
Our study revealed a potentially higher comorbidity rate for GD and CD. However, UC might represent a protective factor for GD. The underlying mechanism and potential common pathways await discovery.
Study context
- Population
- GWAS summary data from Biobank Japan and the International Inflammatory Bowel Disease Genetic Consortium
- Comparison
- Genetically predicted inflammatory bowel disease (IBD) vs Graves disease (GD)
- Outcome
- Causal relationship between GD and IBD
Methodological detailsGWAS summary data, random-effect inverse variance weighted, weighted median, MR-Egger regression, MR-PRESSO
- GWAS summary data
- Random-effect inverse variance weighted, weighted median, MR-Egger regression, MR-PRESSO
Main finding
As reported in the abstract
Risk of GD with genetically predicted IBD
Genetically predicted IBD may increase risk of GD by 24%: OR (95% CI), P
1.24
1.01–1.52P = .041
Further findings
Crohn disease (CD) and ulcerative colitis (UC) and risk of GD
- CD may increase the risk of GD, whereas UC may prevent developing GD
Genetically predicted GD and risk of CD, UC or IBD
- GD may slightly increase the risk of CD; evidence that GD increased the risk of UC or IBD was lacking
Outlier-corrected analysis
- Outlier-corrected results were consistent with raw causal estimates
Original publication
Graves Disease and Inflammatory Bowel Disease: A Bidirectional Mendelian Randomization. J Clin Endocrinol Metab. Published 2 December 2022. doi:10.
Composed by AI from the published abstract and checked against it. How Briefs are made →