Autoimmune myasthenia gravis.
The evident defect in this disease is postsynaptic dysfunction due to anti-acetylcholine receptor antibodies. The postsynaptic membrane is simplified, the number of acetylcholine receptors is reduced, and neuromuscular transmission is impaired. Antiacetylcholinesterase drugs still play a role in management. Newer options include prednisone, azathioprine, and cyclosporine.
Washington University, St. Louis.
G
G
Lopate
A
A
Pestronk
D000328:Adult; D000367:Age Factors; D000917:Antibody Formation / Q000276:immunology; D001327:Autoimmune Diseases / Q000175:diagnosis / Q000276:immunology / Q000628:therapy; D016572:Cyclosporine / Q000009:adverse effects / Q000627:therapeutic use; D003937:Diagnosis, Differential; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000009:adverse effects / Q000627:therapeutic use; D007231:Infant, Newborn; D008297:Male; D009157:Myasthenia Gravis / Q000175:diagnosis / Q000276:immunology / Q000628:therapy; D009469:Neuromuscular Junction; D010956:Plasmapheresis; D011241:Prednisone / Q000009:adverse effects / Q000627:therapeutic use; D011729:Pyridostigmine Bromide / Q000009:adverse effects / Q000627:therapeutic use; D011950:Receptors, Cholinergic / Q000276:immunology; D009435:Synaptic Transmission; D013934:Thymectomy; D013950:Thymus Gland / Q000276:immunology / Q000601:surgery
D016756:Immunoglobulins, Intravenous; D011950:Receptors, Cholinergic; D016572:Cyclosporine; D011729:Pyridostigmine Bromide; D011241:Prednisone