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肌无力危象在临床上是专指重症肌无力(MG)发生严重呼吸困难而危及生命的紧急状态,常同时伴有全身肌肉无力;可造成很高的死亡率(如Osserman为43.3％,吕传真等为57％,薛肇坚为48.4％)。 MG自1960年Simpson提出自体免疫疾病假说后,近十年来已证明本病的基本病变是突触后膜菸碱型乙酰胆碱受体(nAchR)缺陷而造成的神经肌肉传递障碍(Aguago A J等1979)。Drachmann等发现MG病人每个接头的AchR数目比对照组减少70～80％,他与Vincent等(1980)共同认为神经肌肉接头处有效乙酰胆碱受体数目减少,抗AchR抗体增高,是引起肌无力的机理所在。涂来慧等(1981),因在动物血清中测得抗nAchR的抗体。而进一步证明本病属自体免疫性疾病。
Myasthenia gravis is clinically defined as myasthenia gravis (MG), a serious, life-threatening emergency that is accompanied by generalized muscle weakness; it can cause very high rates of death (eg Osserman 43.3%, Lu Fax 57%, Xue Zhajian 48.4%). Since Simpson’s hypothesis of autoimmune disease was proposed by Simpson in 1960, the basic disease of this disease has been proved to be a neuromuscular delivery disorder caused by the defect of the postsynaptic nicotinic acetylcholine receptor (nAchR) in the past decade (Aguago AJ et al., 1979) . Drachmann et al. Found that the number of AchRs per linker in MG patients was reduced by 70-80% compared with that in the control group. He and Vincent et al. (1980) shared the view that the number of effective acetylcholine receptors at the neuromuscular junction was decreased and the anti-AchR antibody was increased Mechanism. Tu Hui et al (1981), because of the anti-nAchR antibodies measured in animal serum. And further evidence that the disease is an autoimmune disease.