Honnorat Jérôme
Bull Acad Natl Med. 2014 Feb;198(2):243-54; discussion 255.
Lambert-Eaton myasthenic syndrome (LEMS) is a rare autoimmune disorder affecting neuromuscular junctions. LEMS has served as a model of paraneoplastic neurological syndromes and antitumoral immunity, shedding light on the pathological role of autoantibodies directed against synaptic targets. Autoantibodies associated with LEMS are directed against voltage-gated calcium channels (VGCC) present on nerve terminals of neuromuscular synapses. Anti-VGGC antibodies play a direct pathological role in LEMS by blocking VGCC and calcium entry during depolarisation. Nearly half of patients with LEMS have small-cell lung cancer (SCLC), which also expresses VGCC. Diagnosis of LEMS frequently permits early detection and treatment of SCLC Knowledge of this syndrome has led to the discovery of a broad range of cancerous and non cancerous antibody-mediated neurological syndromes, and led to the concept of autoimmune synaptopathies.
兰伯特-伊顿肌无力综合征(LEMS)是一种罕见的影响神经肌肉接头的自身免疫性疾病。LEMS已成为副肿瘤性神经综合征和抗肿瘤免疫的模型,为针对突触靶点的自身抗体的病理作用提供了线索。与LEMS相关的自身抗体针对神经肌肉突触神经末梢上的电压门控钙通道(VGCC)。抗VGGC抗体通过在去极化过程中阻断VGCC和钙内流,在LEMS中发挥直接的病理作用。近一半的LEMS患者患有小细胞肺癌(SCLC),后者也表达VGCC。LEMS的诊断常常有助于SCLC的早期发现和治疗。对该综合征的认识促使人们发现了广泛的癌症性和非癌症性抗体介导的神经综合征,并催生了自身免疫性突触病的概念。