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重症肌无力(简称MG)自1672年Willis首先描述本病以来已有数百年历史,近年来在其免疫机制、遗传因素等方面有较深入的研究,治疗则由单一的抗胆碱酯酶剂发展到多个方面,现分述如下。免疫机制及遗传因素的研究自1959年Smither 根据MG 病人的胸腺和甲状腺炎病人的甲状腺组织学相似而提出本病可能为自身免疫病后,对MG 的研究已集中于免疫系统,现多认为导致患者神经肌肉传导受损的主要原因是抗AchR 抗体的产生,85～90%患者具有此抗体,其患病肌肉的AchR 数目减少,IgG 被固定在残留受体表面并进一步加速其破坏,从而损害了神经肌肉传导。AchR 抗体的产生认为与胸腺有关,约75%患者有胸腺异常,15%有胸腺瘤。胸腺病理改变为本
Myasthenia gravis (referred to as MG) since 1672 Willis first described the disease has been hundreds of years of history, in recent years in its immune mechanism, genetic factors have more in-depth study, the treatment by a single anticholinergic agent development To many aspects, are as follows. Immune mechanism and genetic factors since 1959 Smither MG thyroid and thyroid patients according to thyroid histology similar to the proposed disease may be autoimmune disease, the study of MG has focused on the immune system, is now considered to lead to The main cause of impaired neuromuscular conduction in patients is the production of anti-AchR antibodies, which are present in 85-90% of patients and reduce the number of AchR in diseased muscle, immobilize IgG on the surface of residual receptors and further damage their destruction, Neuromuscular conduction. The production of AchR antibodies is thought to be related to the thymus, with about 75% having thymus abnormalities and 15% having thymoma. Thymus-based pathological changes