Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 740-744 |
| Number of pages | 5 |
| Journal | Annals of neurology |
| Volume | 20 |
| Issue number | 6 |
| DOIs | |
| State | Published - Dec 1986 |
ASJC Scopus subject areas
- Neurology
- Clinical Neurology