Evidence map›Paper›PMID 39340433›Full record

ArticleEpilepsia open2024

Systemic lupus erythematosus and epilepsy: A Mendelian randomization study.

Yang Hu, Duo Lin, Dongmei Wu, Yuqing Zhang, Gongbo Li

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Article in Epilepsia open, 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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3citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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3 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Yang HuDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Duo LinDepartment of Neurology, Zhongshan Hospital of Traditional Chinese Medicine, Guangdong, China.
Dongmei WuDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Yuqing ZhangDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.ORCID https://orcid.org/0000-0003-0451-4597
Gongbo LiDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Funding

China Postdoctoral Science Foundation 2022M710562Kuanren Talents Program of the second affiliated Hospital of Chongqing Medical University kryc-yq-2215Natural Science Foundation of China 82001434Natural Science Foundation of Chongqing CSTB2023NSCQ-MSX0176Natural Science Foundation of Chongqing cstc2020jcyj-msxmX0149
6 · The paper itself

Abstract

objectiveNumerous observational studies have found a relationship between systemic lupus erythematosus (SLE) and epilepsy; however, their causal relationship remains unclear. This study aimed to investigate the causal role of SLE in epilepsy or any of its subtypes using a two-sample Mendelian randomization (MR) analysis.

methodsSingle nucleotide polymorphisms (SNPs) linked to SLE were utilized as instrumental variables in MR analysis to assess their causal impact on epilepsy. The primary MR findings were derived using the inverse variance weighted (IVW) method, which was further supported by the weighted median and MR-Egger regression techniques. Additionally, sensitivity analyses, including Cochran's Q test and pleiotropy tests, were conducted to evaluate the influence of these SNPs on epilepsy, particularly looking for signs of horizontal pleiotropy and heterogeneity.

resultsWe selected 43 SNPs that reached genome-wide significance from genome-wide association studies (GWASs) on SLE to serve as instrumental variables in this study. The IVW method showed no evidence to support a causal association between SLE and epilepsy (all epilepsy: odds ratio (OR) = 1.006, 95% confidence interval (CI) = 0.994-1.018; focal epilepsy: OR = 1.006, 95% CI = 0.994-1.019; generalized epilepsy: OR = 1.015, 95% CI = 0.996-1.035). Other MR complementary methods revealed consistent results. Furthermore, there was no evidence indicating heterogeneity or horizontal pleiotropy. SIGNIFICANCE: The findings of MR analysis did not support a genetically predicted causal relationship between SLE and epilepsy, but emphasized the need for further research on shared pathophysiological mechanisms, particularly the role of immune system abnormalities and potential influences such as chronic inflammation and therapeutic interventions. PLAIN LANGUAGE SUMMARY: The etiology of epilepsy is complex and diverse, including immune factors. Through a Mendelian randomization analysis, we did not find evidence of a genetic causal relationship between systemic lupus erythematosus and epilepsy. However, this does not invalidate epidemiological evidence, and further exploration is needed to investigate factors influencing the relationship between the two.

Indexed as

EpilepsyGenome-Wide Association StudyLupus Erythematosus, SystemicMendelian Randomization AnalysisPolymorphism, Single NucleotideGenetic Predisposition to DiseaseHumansepilepsyMendelian randomizationsystemic lupus erythematosus

Identifiers

PMID39340433
PMCPMC11633673

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