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Muscle Nerve. 2013 Jun;47(6):928-30. doi: 10.1002/mus.23751. Epub 2013 May 11.

Exacerbation of myasthenia gravis with voriconazole.

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1
Neuromuscular Center, Department of Neurology and Neurological Institute, University Hospitals Case Medical Center, 11100 Euclid Avenue, Cleveland, Ohio 44106-5098, USA.

Abstract

INTRODUCTION:

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.

PMID:
23666793
DOI:
10.1002/mus.23751
[Indexed for MEDLINE]
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