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Epilepsy in systemic lupus erythematosus: prevalence and risk factors

医学 癫痫 抗磷脂综合征 狼疮抗凝剂 自身抗体 内科学 抗核抗体 人口 痹症科 队列 病因学 精神病 儿科 免疫学 精神科 抗体 血栓形成 环境卫生
作者
L Hopia,Magnus Andersson,Elisabet Svenungsson,Mohsen Khademi,Fredrik Piehl,Torbjörn Tomson
出处
期刊:European Journal of Neurology [Wiley]
卷期号:27 (2): 297-307 被引量:22
标识
DOI:10.1111/ene.14077
摘要

Background and purpose The aim was to study the prevalence of epilepsy in a hospital‐based systemic lupus erythematosus ( SLE ) cohort and to investigate the relationship between epilepsy and other manifestations of neuropsychiatric SLE ( NPSLE ). Methods The study population consisted of 440 SLE patients recruited from 1998 to 2012. An epilepsy‐screening questionnaire was sent to all patients, where those screening positive were invited to a neurological examination with documentation of NPSLE symptoms according to the American College of Rheumatology nomenclature. Occurrences of autoantibodies (double stranded DNA antibody, antinuclear antibody, lupus anticoagulant, Sjögren's syndrome A, Sjögren's syndrome B) and the antiphospholipid syndrome ( APS ) were tabulated. Results Out of 440 patients, 14% were dead and 2.7% were lost to follow‐up. The questionnaire was sent to 368 patients; 312 (85%) responded. Of these, 131 (42%) screened positive. Epilepsy was confirmed in 36 (11.5%), of whom 30 (83%) had focal onset. Ten (3.2%) patients had isolated or provoked seizures. Manifestations of NPSLE occurred in 50%. The rates of cerebrovascular disease and psychosis were elevated two‐ and three‐fold in NPSLE patients with epilepsy versus NPSLE patients without epilepsy, respectively ( P = 0.001 and P = 0.0006). APS was more common in patients with epilepsy compared to epilepsy‐free SLE patients with or without NPSLE ( P = 0.02). In 50% of patients with epilepsy, no other etiology than SLE was detected. Conclusions A high prevalence of epilepsy in SLE patients is reported, with association to concurrent cerebrovascular disease, APS and psychosis. Our findings support the notion of a multifactorial background for epilepsy in SLE including both vascular disease and features consistent with autoimmunity.

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