atorvastatin/pravastatin

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Reactions 1228 - 15 Nov 2008 S Atorvastatin/pravastatin Myasthenia gravis: case report A 43-year-old man with hyperlipidaemia, who had experienced a myocardial infarction (MI), developed myasthenia gravis during treatment with atorvastatin. He subsequently experienced a recurrence of myasthenia gravis during treatment with pravastatin [dosage not stated]. The man, who also had diabetes mellitus, developed diffuse myalgia soon after starting treatment with atorvastatin 10 mg/day. His myalgia worsened when atorvastatin was subsequently increased to 20 mg/day, and he developed bilateral blepharoptosis. One year later, following another MI, atorvastatin was increased to 40 mg/day. Two to 3 weeks later, he experienced double vision and worsening blepharoptosis. Myasthenia gravis was suspected. The man was treated with IV edrophonium and his blepharoptosis improved. A subsequent investigation revealed an elevated acetylcholine receptor antibody (Anti-AchR) level of 10.8 nmol/L, a titin level of 6.2 and an antibody titre against parietal cells of 1024. Single fibre electromyography revealed increased jitter and blocking in 24/30 pairs; the mean value of the consecutive differences was just above normal. Treatment with IV immunoglobulins, azathioprine, pyridostigmine and plasma exchange did not improve his condition. Atorvastatin was considered a suspect 2 years after his first symptoms and the agent was discontinued. His myalgia rapidly recovered and, within a few days, his blepharoptosis had completely resolved. He continued to experience diplopia. Repeat tests revealed a normal Anti-AchR level 6 months after discontinuing atorvastatin, but the AchR level remained slightly elevated during the subsequent follow-up period. The man experienced another MI 1 year after discontinuing atorvastatin. He was started on pravastatin and his blepharoptosis soon recurred. Pravastatin was discontinued and his blepharoptosis immediately improved. However, he experienced a worsening of his blepharoptosis and diplopia when pravastatin was reintroduced. Pravastatin was again discontinued and he subsequently started treatment with ezetimibe. He did not experience a recurrence of muscular complaints and his blepharoptosis resolved. His diplopia remained remarkably stable and was surgically treated after 2 years. Author comment: "AchR antibody remained at a slightly elevated level without statin, which could support a theory that this patient had an underlying [myasthenia gravis] exacerbated by statin use. However, during a 3-year observation period after statin withdrawal, he revealed no myasthenic symptom." Elsais A, et al. Ptosis, diplopia and statins: an association? European Journal of Neurology 15: e92-e93, No. 10, Oct 2008 - Norway 801124594 1 Reactions 15 Nov 2008 No. 1228 0114-9954/10/1228-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

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Page 1: Atorvastatin/pravastatin

Reactions 1228 - 15 Nov 2008

SAtorvastatin/pravastatin

Myasthenia gravis: case reportA 43-year-old man with hyperlipidaemia, who had

experienced a myocardial infarction (MI), developedmyasthenia gravis during treatment with atorvastatin. Hesubsequently experienced a recurrence of myasthenia gravisduring treatment with pravastatin [dosage not stated].

The man, who also had diabetes mellitus, developed diffusemyalgia soon after starting treatment withatorvastatin 10 mg/day. His myalgia worsened whenatorvastatin was subsequently increased to 20 mg/day, and hedeveloped bilateral blepharoptosis. One year later, followinganother MI, atorvastatin was increased to 40 mg/day. Two to 3weeks later, he experienced double vision and worseningblepharoptosis. Myasthenia gravis was suspected.

The man was treated with IV edrophonium and hisblepharoptosis improved. A subsequent investigation revealedan elevated acetylcholine receptor antibody (Anti-AchR) levelof 10.8 nmol/L, a titin level of 6.2 and an antibody titre againstparietal cells of 1024. Single fibre electromyography revealedincreased jitter and blocking in 24/30 pairs; the mean value ofthe consecutive differences was just above normal. Treatmentwith IV immunoglobulins, azathioprine, pyridostigmine andplasma exchange did not improve his condition. Atorvastatinwas considered a suspect 2 years after his first symptoms andthe agent was discontinued. His myalgia rapidly recoveredand, within a few days, his blepharoptosis had completelyresolved. He continued to experience diplopia. Repeat testsrevealed a normal Anti-AchR level 6 months afterdiscontinuing atorvastatin, but the AchR level remainedslightly elevated during the subsequent follow-up period.

The man experienced another MI 1 year after discontinuingatorvastatin. He was started on pravastatin and hisblepharoptosis soon recurred. Pravastatin was discontinuedand his blepharoptosis immediately improved. However, heexperienced a worsening of his blepharoptosis and diplopiawhen pravastatin was reintroduced. Pravastatin was againdiscontinued and he subsequently started treatment withezetimibe. He did not experience a recurrence of muscularcomplaints and his blepharoptosis resolved. His diplopiaremained remarkably stable and was surgically treated after2 years.

Author comment: "AchR antibody remained at a slightlyelevated level without statin, which could support a theorythat this patient had an underlying [myasthenia gravis]exacerbated by statin use. However, during a 3-yearobservation period after statin withdrawal, he revealed nomyasthenic symptom."Elsais A, et al. Ptosis, diplopia and statins: an association? European Journal ofNeurology 15: e92-e93, No. 10, Oct 2008 - Norway 801124594

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Reactions 15 Nov 2008 No. 12280114-9954/10/1228-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved