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Exacerbation of myasthenia gravis with voriconazole
Author(s) -
Azzam Raed,
Shaikh Aasef G.,
Serra Alessandro,
Katirji Bashar
Publication year - 2013
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.23751
Subject(s) - voriconazole , myasthenia gravis , plasmapheresis , exacerbation , ptosis , medicine , neuromuscular junction , acetylcholine receptor , pharmacology , immunology , receptor , antibody , biology , dermatology , neuroscience , antifungal
We describe a patient with stable generalized myasthenia gravis who presented with new onset severe ophthalmoplegia and ptosis after initiation of voriconazole for aspergillosis. Methods Ligand‐protein docking software was used to simulate the interaction of voriconazole with the acetylcholine receptor ( AChR ). We tested voriconazole binding to AChR in comparison to high affinity and neutral compounds. Results There was no clinical improvement after intravenous immunoglobulin infusion and plasmapheresis. However, the patient improved slowly after withdrawal of voriconazole. Based on our results, voriconazole binds favorably to AChR and may putatively block muscle nicotinic AChRs . Other theoretical explanations include blocking potassium channels and reducing their intracellular trafficking. Conclusions The mechanisms involved in ocular exacerbation may be multi‐factorial, reflecting the intricate dynamics of the neuromuscular junction. It is important to consider medications that harbor pyridine or pyrimidine moieties as potential causes of exacerbation in myasthenic patients, especially those who present with ocular symptoms. Muscle Nerve 47: 928–930, 2013