Kuncl R W, Pestronk A, Drachman D B, Rechthand E
Ann Neurol. 1986 Dec;20(6):740-4. doi: 10.1002/ana.410200617.
The temporal course and pathophysiology of penicillamine-induced myasthenia gravis were studied in detail in a typical case. Our results suggest that this disorder and idiopathic autoimmune myasthenia gravis share the same essential pathophysiological features, including the presence of anti-acetylcholine receptor (AChR) antibody, serum-induced blockade of AChRs, antibody-mediated accelerated degradation of AChRs, and a resultant quantitative reduction in available junctional AChRs. An initial severe reduction in junctional AChRs was reversed and the patient recovered, both within 8 months of stopping penicillamine. Our data suggest that penicillamine probably produced myasthenia gravis by initiating a new autoimmune response rather than by enhancing ongoing autoimmunity.
