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NEUROLOGY 1980;30:1246
© 1980 American Academy of Neurology

Penicillamine-associated myasthenia gravis

James W. Albers, M.D., Ph.D., Richard J. Hodach, M.D., Ph.D., David W. Kimmel and William L. Treacy, M.D.

Departments of Neurology (Drs. Albers and Hodach and Mr. Kimmel) and Internal Medicine, Division of Rheumatology (Dr. Treacy), Medical College of Wisconsin, Milwaukee County Medical Complex, and the Department of Medicine (Dr. Treacy), St. Joseph Hospital, Milwaukee, WI.

Electroneuromyographic studies have been reported as abnormal in only 9 of 23 cases of penicillamine-associated myasthenia gravis (MG). We report a patient with rheumatoid arthritis who developed clinical and electrodiagnostic evidence of myasthenia 7 months after beginning penicillamine therapy. Six months after discontinuing penicillamine, it was possible to discontinue anticholinesterase medications. With clinical improvement, electrodiagnostic studies (including single-fiber electrmyography) improved, serum antibody titers to human muscle acetylcholine receptor fell, and lymphocytes became more responsive to the nonspecific mitogen phytohemagglutinin. Evidence suggests that penicillamine-associated myasthenia is a distinct syndrome rather than the chance occurrence of two diseases. This syndrome is clinically and electrophysiologically distinguishable from idiopathic myasthenia only by the high remission rate after penicillamine is discontinued.

Address correspondence and reprint requests to Dr. Albers, Department of Neurology, University of Michigan Medical Center, B4917 Clinical Faculty Office Building, Ann Arbor, MI 48109.

Accepted for publication December 26, 1979.

This work was presented in part at the twenty-sixth annual meeting of the American Association of Electromyography and Electrodiagnosis, New Orleans, LA, October 1979.




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