Herrmann C, Lindstrom J M, Keesey J C, Mulder D G
West J Med. 1985 Jun;142(6):797-809.
An edited summary of an Interdepartmental Conference arranged by the Department of Medicine of the UCLA School of Medicine, Los Angeles. The Director of Conferences is William M. Pardridge, MD, Associate Professor of Medicine. Current findings indicate that autoimmune myasthenia gravis is an acquired immune complex disorder of neuromuscular transmission in voluntary striated muscle. There is a break in immunologic tolerance leading to blocking and degradation of acetylcholine receptors, together with widening of the synaptic cleft associated with partial destruction, simplification and shortening of the postjunctional membrane. Thymic hyperplasia and thymoma may be present. A decremental response to nerve-muscle stimulation, blocking and jitter on single-fiber electromyography and circulating antibodies to acetylcholine receptor are detectable in most patients with generalized weakness. Although the cause of this abnormal immunologic mechanism remains to be discovered, anticholinesterases, corticosteroids, immunosuppressants, plasmapheresis or thymectomy (individually or in combination) provide control and better prognosis in most patients.
这是洛杉矶加州大学洛杉矶分校医学院医学系组织的一次跨部门会议的编辑摘要。会议主任是医学副教授威廉·M·帕德里奇医学博士。目前的研究结果表明,自身免疫性重症肌无力是一种获得性免疫复合物介导的随意横纹肌神经肌肉传递障碍性疾病。免疫耐受出现破坏,导致乙酰胆碱受体被阻断和降解,同时突触间隙增宽,伴有突触后膜部分破坏、简化和缩短。可能存在胸腺增生和胸腺瘤。大多数全身无力的患者可检测到对神经肌肉刺激的递减反应、单纤维肌电图上的阻滞和颤抖以及抗乙酰胆碱受体循环抗体。尽管这种异常免疫机制的原因仍有待发现,但抗胆碱酯酶、皮质类固醇、免疫抑制剂、血浆置换或胸腺切除术(单独或联合使用)可使大多数患者得到控制并获得较好的预后。