D-penicillamine has been used in the treatment of rheumatoid arthritis
for years. As a rare complication of this treatment the occurrence of
myasthenia gravis has been described, the clinical features of this c
omplication being indistinguishable from that of idiopathic myasthenia
gravis. Both D-penicillamine induced and idiopathic myasthenia gravis
show elevated titers of acetylcholine receptor antibodies and respond
to acetylcholinesterase inhibitor treatment. We report on a patient w
ith rheumatoid arthritis who, under treatment with D-penicillamine, de
veloped severe myasthenia gravis which required temporary acetylcholin
esterase inhibitor therapy. 8 months after D-penicillamine was discont
inued the acetylcholine receptor antibodies had disappeared and the ac
etylcholinesterase inhibitors could be withdrawn. Clinical findings an
d possible pathogenetic aspects of D-penicillamine induced myasthenia
gravis are discussed.