Abstract <p>Uric acid (UA) is essential in the physiological and pathophysiological processes of various diseases. The linkage between serum uric acid (SUA) levels and epilepsy has been investigated by observational studies. However, these findings are susceptible to confounding factors, making the causal relationship unelucidated. This project aimed to apply Mendelian randomization (MR) to clarify the causal linkage between SUA and epilepsy. We utilized data from GWAS and the UK Biobank to analyze the causal link between SUA and epilepsy by utilizing the two-sample bidirectional MR method. Additionally, SUA data from the Global Urate Genetics Consortium and epilepsy data from the International League Against Epilepsy were included as validation sets. The two-sample bidirectional MR analysis yielded no evidence of a causal relationship between SUA and epilepsy. Similar results were generated by analyzing the validation set data. Sensitivity analysis and heterogeneity test confirmed that there was no pleiotropy or heterogeneity in instrumental variables. The MR results of this project were robust. Our project does not give compelling evidence of a significant causal link between SUA and epilepsy.</p>

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Assessment of the Causality between Uric Acid and Epilepsy: Bidirectional Two-Sample Mendelian Randomization

  • Yan Wang,
  • Ling Chen

摘要

Abstract

Uric acid (UA) is essential in the physiological and pathophysiological processes of various diseases. The linkage between serum uric acid (SUA) levels and epilepsy has been investigated by observational studies. However, these findings are susceptible to confounding factors, making the causal relationship unelucidated. This project aimed to apply Mendelian randomization (MR) to clarify the causal linkage between SUA and epilepsy. We utilized data from GWAS and the UK Biobank to analyze the causal link between SUA and epilepsy by utilizing the two-sample bidirectional MR method. Additionally, SUA data from the Global Urate Genetics Consortium and epilepsy data from the International League Against Epilepsy were included as validation sets. The two-sample bidirectional MR analysis yielded no evidence of a causal relationship between SUA and epilepsy. Similar results were generated by analyzing the validation set data. Sensitivity analysis and heterogeneity test confirmed that there was no pleiotropy or heterogeneity in instrumental variables. The MR results of this project were robust. Our project does not give compelling evidence of a significant causal link between SUA and epilepsy.