Kampylafka E I, Alexopoulos H, Fouka P, Moutsopoulos H M, Dalakas M C, Tzioufas A G
Department of Pathophysiology, Faculty of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Department of Pathophysiology, Faculty of Medicine, National and Kapodistrian University of Athens, Athens, Greece Department of Neurology, Thomas Jefferson University, Philadelphia, USA.
Lupus. 2016 Oct;25(11):1260-5. doi: 10.1177/0961203316636473. Epub 2016 Feb 27.
We investigated systemic lupus erythematosus (SLE) patients with epilepsy, a major and organic neurological symptom. Our aim was to test patients for the autoimmune epilepsy-associated antibodies anti-GAD, anti-NMDAR, anti-AMPAR1/2, anti-GABABR and anti-VGKC. We tested sera from ten SLE patients with current or previous episodes of epileptic seizures. In addition, sera were tested for staining on primary hippocampal neurons. The patients' clinical and neuroimaging profile, disease activity and accumulated damage scores and therapeutic regimens administered were recorded, and correlations were evaluated. Patients were negative for all anti-neuronal autoantibodies tested, and showed no staining on primary hippocampal cells, which suggests the absence of autoantibodies against neuronal cell surface antigens. Epileptic seizures were all tonic-clonic, and all patients had high disease activity (mean SLE Damage Acticity Index score 19.3 ± 7.3). Six patients had minor or no brain magnetic resonance imaging findings, and three had major findings. 9/10 patients received immunosuppression for 5 ± 4 months, while anti-convulsive treatment was administered to all patients (4.2 ± 3 years). Our results suggest that the majority of SLE-related epileptic seizures cannot be attributed to the action of a single antibody against neuronal antigens. Studies with larger neuropsychiatric SLE populations and stricter inclusion criteria are necessary to verify these findings.
我们对患有癫痫（一种主要的器质性神经症状）的系统性红斑狼疮（SLE）患者进行了调查。我们的目的是检测患者是否存在与自身免疫性癫痫相关的抗体，即抗谷氨酸脱羧酶（anti-GAD）、抗N-甲基-D-天冬氨酸受体（anti-NMDAR）、抗α-氨基-3-羟基-5-甲基-4-异恶唑丙酸受体1/2（anti-AMPAR1/2）、抗γ-氨基丁酸B型受体（anti-GABABR）和抗电压门控钾通道复合体（anti-VGKC）。我们检测了10名有当前或既往癫痫发作史的SLE患者的血清。此外，还检测了血清对原代海马神经元的染色情况。记录了患者的临床和神经影像学特征、疾病活动度和累积损伤评分以及所采用的治疗方案，并评估了相关性。所有检测的抗神经元自身抗体在患者中均为阴性，并且在原代海马细胞上未显示染色，这表明不存在针对神经元细胞表面抗原的自身抗体。癫痫发作均为强直阵挛性发作，所有患者疾病活动度都很高（平均SLE损伤活动指数评分为19.3±7.3）。6名患者脑部磁共振成像检查结果轻微或无异常，3名患者有明显异常。10名患者中有9名接受了5±4个月的免疫抑制治疗，而所有患者均接受了抗惊厥治疗（4.2±3年）。我们的结果表明，大多数与SLE相关的癫痫发作不能归因于针对神经元抗原的单一抗体的作用。有必要对更大的神经精神性SLE人群进行研究，并采用更严格的纳入标准来验证这些发现。
