What drugs should be avoided in myasthenia gravis?
Myasthenia gravis is a rare autoimmune disease occurring in 0.25 to 2 people per 100,000 annually.1,2 Normally, for a synaptic transmission to occur at the neuromuscular junction, an action potential must initiate depolarization of the presynaptic terminal. Once the presynaptic terminal has been depolarized, there is an influx of calcium, which causes the release of acetylcholine from vesicles. The acetylcholine then enters the synaptic cleft and binds to the postsynaptic acetylcholine receptor (AChR). This interaction then causes a depolarization of the postsynaptic terminal, which allows the signal to propagate and eventually ends in stimulation of the muscle. In myasthenia gravis, formation of antibodies directed against the AChR in the postsynaptic neuron form. The antibodies bind with the AChR, thus making acetylcholine unable to complex with the AChR. This causes a decrease in the total number of AChRs and muscle weakness due to diminished neurotransmission to the postsynaptic me
