SynthesisFrontiers in endocrinology2024
The harmful effect of ankylosing spondylitis on diabetes mellitus: new evidence from the Mendelian randomization analysis.
Synthesis in Frontiers in endocrinology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Glucolipid metabolic dysfunction in ankylosing spondylitis: inflammatory mechanisms, immune-metabolic crosstalk and therapeutic implications of natural products and traditional Chinese medicine.Frontiers in immunology · 2026Review
- Causal Risk Factors for Type 1 Diabetes in Mendelian Randomization Studies: A Systematic Review and Meta-Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Age, Gender, and Disease Duration as Key Determinants of Comorbidity Burden in Spondyloarthritis: A Multicentre Cross-Sectional Study.Mediterranean journal of rheumatology · 2025Article
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Authors and funding
6 authors.
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Abstract
Background: While observational research has highlighted a possible link between ankylosing spondylitis (AS) and type 2 diabetes (T2DM), the quality of evidence remains limited, and the causal relationship is yet to be established. This study aims to explore the causal link between AS and T2DM, as well as its impact on traits related to glucose metabolism. Method: To infer a causal relationship between AS and various diabetes-related traits, including type 1 diabetes (T1DM), T2DM, blood glucose levels, fasting glucose, glycated hemoglobin, and fasting insulin, we employed Mendelian randomization (MR) analysis. We sourced GWAS summary data for both exposure and outcome variables from the IEU OpenGWAS database, GWAS Catalog, and FinnGen database. To synthesize the results of the MR analyses, we applied meta-analysis techniques using either a fixed or random effects model. For identifying and excluding instrumental variants (IVs) that exhibit horizontal pleiotropy with the outcomes, we utilized the MR-PRESSO method. Sensitivity analyses were conducted using the MR-Egger method, along with Q and I^2 tests, to ensure the robustness of our findings. Results: Our analysis revealed a significant association between AS and an increased risk of T1DM with an odds ratio (OR) of 1.5754 (95% CI: 1.2935 to 1.9187) and T2DM with an OR of 1.0519 (95% CI: 1.0059 to 1.1001). Additionally, AS was associated with elevated levels of fasting glucose (beta coefficient = 0.0165, 95% CI: 0.0029 to 0.0301) and blood glucose (beta coefficient = 0.0280, 95% CI: 0.0086 to 0.0474), alongside a decrease in fasting insulin levels (beta coefficient = -0.0190, 95% CI: -0.0330 to -0.0050). Conclusion: Our findings collectively underscore the detrimental impact of AS on the development of diabetes, highlighting the critical influence of autoimmune disorders in diabetes onset. This provides profound insights into the pathogenesis of diabetes from an immunological standpoint.
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