Zandman-Goddard Gisele, Chapman Joab, Shoenfeld Yehuda
Lecturer of Internal Medicine, Sackler Faculty of Medicine, Tel-Aviv University, Israel; Head of the Department of Medicine C, Wolfson Medical Center, Holon, Israel.
Semin Arthritis Rheum. 2007 Apr;36(5):297-315. doi: 10.1016/j.semarthrit.2006.11.003. Epub 2007 Jan 26.
We sought (1) to identify and (2) to define the association of all reported antibodies (Abs) with neuropsychiatric lupus (NPSLE), (3) to search for possible mechanisms that are involved in NPSLE, and (4) to determine whether we can recognize a panel of Abs associated with specific neuropsychiatric (NP) manifestations.
A MEDLINE search (1975 to 2005) was performed utilizing the following terms: neuropsychiatric lupus, antiphospholipid syndrome, or central nervous system systemic lupus erythematosus matched with the term antibodies.
Twenty Abs (11 brain-specific and 9 systemic) were described in NPSLE patients. These include Abs that target brain-specific antigens (neuronal, ganglioside, synaptosomes, glia, methyl-d-aspartate receptors, lymphocytotoxic) and systemic antigens (nuclear, cytoplasmic, phospholipid, endothelial cells). Cognitive impairment, psychosis, and depression were associated with many Abs. Elevated titers of anticardiolipin Abs (aCL) were reported most often and found in patients with cognitive impairment, psychosis, depression, seizures, chorea, and migraine. No specificity was encountered among brain-specific or systemic Abs for any single NP manifestation. No studies evaluated a specific NP manifestation with the full panel of 20 Abs. A panel of brain-specific and systemic Abs may be helpful in establishing the diagnosis of NPSLE. Postulated mechanisms in experimental models included vascular occlusion and injury by pathogenic Abs in a disrupted blood brain barrier.
NPSLE is associated with brain-specific and systemic Abs. Cognitive impairment, psychosis, and depression were associated with many Abs, including aCL Abs. Possible mechanisms include vascular occlusion and injury by pathogenic Abs in a disrupted blood brain barrier.
我们旨在（1）识别并（2）定义所有已报道抗体（Abs）与神经精神性狼疮（NPSLE）的关联，（3）探寻参与NPSLE的可能机制，以及（4）确定我们是否能够识别一组与特定神经精神（NP）表现相关的抗体。
利用以下检索词对MEDLINE（1975年至2005年）进行检索：神经精神性狼疮、抗磷脂综合征或中枢神经系统系统性红斑狼疮，并与“抗体”一词匹配。
在NPSLE患者中描述了20种抗体（11种脑特异性抗体和9种系统性抗体）。这些抗体包括靶向脑特异性抗原（神经元、神经节苷脂、突触体、神经胶质、甲基 - D - 天冬氨酸受体、淋巴细胞毒性）和系统性抗原（核、细胞质、磷脂、内皮细胞）的抗体。认知障碍、精神病和抑郁症与多种抗体相关。抗心磷脂抗体（aCL）滴度升高的报道最为常见，且见于认知障碍、精神病、抑郁症、癫痫、舞蹈症和偏头痛患者。在脑特异性或系统性抗体中，未发现对任何单一NP表现具有特异性。没有研究用全部20种抗体评估特定的NP表现。一组脑特异性和系统性抗体可能有助于NPSLE的诊断。实验模型中推测的机制包括血脑屏障破坏时致病性抗体导致的血管闭塞和损伤。
NPSLE与脑特异性和系统性抗体相关。认知障碍、精神病和抑郁症与多种抗体相关，包括aCL抗体。可能的机制包括血脑屏障破坏时致病性抗体导致的血管闭塞和损伤。
