Observational studyMedicine2026
Hyperthyroidism drives gout risk: A Mendelian randomization observational study.
Observational study in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The causal interplay between thyroid dysfunction and gout remains controversial because of confounding and reverse causation in observational studies. Using Mendelian randomization (MR), this study investigated the causal effects of hyperthyroidism and hypothyroidism on the risk of gout. Summary statistics from the UK Biobank and FinnGen genome-wide association study databases were analyzed using 2-sample MR. Genetic instruments for thyroid dysfunction were selected under stringent criteria (P < 5 × 10-8, r2 < 0.001). Causal estimates were derived using inverse-variance weighted regression, supplemented by sensitivity analyses (MR-Egger, weighted median) and bidirectional MR. Genetically predicted hyperthyroidism exhibited a significant positive causal association with gout in both the UK Biobank (OR = 1.215, 95% confidence interval: 1.087-1.332, P = 3.12 × 10-5) and FinnGen cohorts (OR = 1.091, 95% confidence interval: 1.004-1.187, P = .041). No causal link was observed for the hypothyroidism. Bidirectional MR revealed no reverse causality, and sensitivity analyses confirmed robustness against pleiotropy and heterogeneity (P > .05). This study provides genetic evidence that hyperthyroidism is an independent risk factor of gout, indicating a possible unidirectional causal relationship. These findings underscore the necessity of closely monitoring uric acid levels in patients with hyperthyroidism and illuminating specific pathophysiological pathways that warrant further investigation of their underlying mechanisms.
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