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Case ReportOpen Access
Statin-Associated Myasthenic Weakness
Pasutharnchat N 
,
Phanthumchinda K
,
Phanthumchinda K Background: Statin-associated myasthenic weakness is uncommonly recognized. Since 2002, there have been 14 casesdescribed in literatures. However, the underlying mechanism is still unknown.
Case Report: In 2007, a 50-year-old woman with generalized, limb predominated, myasthenia gravis (MG), whose MGstatus has been “minimal manifestation” for several years, developed moderately severe fluctuating bulbar weakness a fewweeks after starting simvastatin 20 mg/day. Simvastatin was discontinued and dosage of cholinesterase inhibitor wastemporarily increased. The symptoms resolved and she was back to her previous status in one month. In 2008, two weeksafter re-challenge with simvastatin 10 mg/day, bulbar weakness re-occurred. Antibody to acetylcholine receptors wasmeasured 4.25 nmole/L. Serum creatine phosphokinase was normal. Electrophysiologic tests showed evidences of postsynapticneuromuscular junction disorder without evidence of myopathy. The symptoms were again resolved after discontinuation ofstatin and temporarily increased dosage of cholinesterase inhibitor. She was back to previous status in two months.Hypercholesterolemia was then controlled with ezetimibe without any worsening in MG status.
Conclusion: Because of the wide use of statins in clinical practice, physicians should be aware of this potential adverse effect.The incidence of statin-associated myasthenic weakness should be clearly investigated. Challenge with other brands of statinor with reduced dosage is not beneficial in these patients. Non-pharmacological treatment and non-statin medication may beconsidered.
Keywords: Statin, Myasthenia gravis, Statin-associated myasthenic weakness
Case Report: In 2007, a 50-year-old woman with generalized, limb predominated, myasthenia gravis (MG), whose MGstatus has been “minimal manifestation” for several years, developed moderately severe fluctuating bulbar weakness a fewweeks after starting simvastatin 20 mg/day. Simvastatin was discontinued and dosage of cholinesterase inhibitor wastemporarily increased. The symptoms resolved and she was back to her previous status in one month. In 2008, two weeksafter re-challenge with simvastatin 10 mg/day, bulbar weakness re-occurred. Antibody to acetylcholine receptors wasmeasured 4.25 nmole/L. Serum creatine phosphokinase was normal. Electrophysiologic tests showed evidences of postsynapticneuromuscular junction disorder without evidence of myopathy. The symptoms were again resolved after discontinuation ofstatin and temporarily increased dosage of cholinesterase inhibitor. She was back to previous status in two months.Hypercholesterolemia was then controlled with ezetimibe without any worsening in MG status.
Conclusion: Because of the wide use of statins in clinical practice, physicians should be aware of this potential adverse effect.The incidence of statin-associated myasthenic weakness should be clearly investigated. Challenge with other brands of statinor with reduced dosage is not beneficial in these patients. Non-pharmacological treatment and non-statin medication may beconsidered.
Keywords: Statin, Myasthenia gravis, Statin-associated myasthenic weakness
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