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已发表论文
肝功能与卒中后癫痫风险的相关性
Received 25 March 2025
Accepted for publication 6 September 2025
Published 8 November 2025 Volume 2025:18 Pages 7375—7382
DOI https://doi.org/10.2147/JMDH.S530478
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Pavani Rangachari
Yu Zhang, Xi Chen
Yixing People’s Hospital, Wuxi, Jiangsu, 214200, People’s Republic of China
Correspondence: Xi Chen, Yixing People’s Hospital, No. 1588 Xincheng Road, Yixing, Wuxi, Jiangsu, People’s Republic of China, Email staff1890@yxph.com
Background: Abnormal liver function has often been associated with epilepsy, but there is a lack of large-scale clinical evidence to support the potential correlation between liver function and post-stroke epilepsy.
Objective: We aimed to explore a real correlation between liver function and secondary epilepsy after stroke.
Methods: From the Dryad database, we retrospectively identified 21,459 patients who had experienced acute ischemic stroke. Multivariate regression was used to clarify the correlation between liver function and secondary epilepsy post-stroke via cross-sectional analysis.
Results: Our multivariate nonlinear analysis, adjusted for age and gender, suggested that a significant correlation exists between liver function (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and the risk of secondary epilepsy post-stroke. Saturation effect analysis showed that a fold point (K) of blood AST level of 39.3 U/L was related to an epilepsy event. An increased AST level was related to a higher rate of epilepsy (1.2 [1.2– 1.3], < 0.001) among patients with AST levels of less than 39.3 U/L. Significance was weaker among patients with AST levels of more than 39.3 U/L. As for ALT, the fold point of blood ALT level revealed an association with epilepsy at 23.3 U/L. Similarly, elevated AST levels were related to a significantly higher risk of secondary epilepsy post-stroke (1.2 [1.1– 1.2], < 0.001) when they were less than 23.3 U/L. The significant correlation was weaker when blood AST levels were higher than 23.3 U/L. Importantly, ROC curve analysis displayed a high AUC value (0.8101) of blood AST in terms of detecting epilepsy risk, with a sensitivity of 0.7254 and specificity of 0.7997, respectively.
Conclusion: Our study provided potential evidence for the correlation between liver function and secondary epilepsy after acute stroke, indicating that early protection and management of liver dysfunction among post-stroke patients might be beneficial for reducing epileptic seizures. More studies with a high level of evidence are needed to confirm this finding, however.
Keywords: secondary epilepsy, hepatic insufficiency, ischemic stroke, diagnostic value, prognosis
Yixing People’s Hospital, Wuxi, Jiangsu, 214200, People’s Republic of China
Correspondence: Xi Chen, Yixing People’s Hospital, No. 1588 Xincheng Road, Yixing, Wuxi, Jiangsu, People’s Republic of China, Email staff1890@yxph.com
Background: Abnormal liver function has often been associated with epilepsy, but there is a lack of large-scale clinical evidence to support the potential correlation between liver function and post-stroke epilepsy.
Objective: We aimed to explore a real correlation between liver function and secondary epilepsy after stroke.
Methods: From the Dryad database, we retrospectively identified 21,459 patients who had experienced acute ischemic stroke. Multivariate regression was used to clarify the correlation between liver function and secondary epilepsy post-stroke via cross-sectional analysis.
Results: Our multivariate nonlinear analysis, adjusted for age and gender, suggested that a significant correlation exists between liver function (alanine aminotransferase [ALT] and aspartate aminotransferase [AST]) and the risk of secondary epilepsy post-stroke. Saturation effect analysis showed that a fold point (K) of blood AST level of 39.3 U/L was related to an epilepsy event. An increased AST level was related to a higher rate of epilepsy (1.2 [1.2– 1.3], < 0.001) among patients with AST levels of less than 39.3 U/L. Significance was weaker among patients with AST levels of more than 39.3 U/L. As for ALT, the fold point of blood ALT level revealed an association with epilepsy at 23.3 U/L. Similarly, elevated AST levels were related to a significantly higher risk of secondary epilepsy post-stroke (1.2 [1.1– 1.2], < 0.001) when they were less than 23.3 U/L. The significant correlation was weaker when blood AST levels were higher than 23.3 U/L. Importantly, ROC curve analysis displayed a high AUC value (0.8101) of blood AST in terms of detecting epilepsy risk, with a sensitivity of 0.7254 and specificity of 0.7997, respectively.
Conclusion: Our study provided potential evidence for the correlation between liver function and secondary epilepsy after acute stroke, indicating that early protection and management of liver dysfunction among post-stroke patients might be beneficial for reducing epileptic seizures. More studies with a high level of evidence are needed to confirm this finding, however.
Keywords: secondary epilepsy, hepatic insufficiency, ischemic stroke, diagnostic value, prognosis