Statin-associated exacerbation of myasthenia gravis

Abstract

Myasthenia gravis (MG) can be exacerbated by a variety of medications, which increase weakness by interrupting neuromuscular junction transmission. Statins, which lower lipids by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, are not commonly known to worsen MG or have activity against the neuromuscular junction. 1 One report suggested that statin therapy produced ocular myasthenia. 2 However, based on the case description, it is not clear that this patient had MG. 3 We present a patient with well-documented MG who experienced worsening of his condition after taking different statins on four separate occasions.Case report. A 55-year-old man with hyperlipidemia and borderline hypertension was evaluated for a 1-year history of intermittent dysarthria. He first noticed dysarthria~1 week after the initiation of atorvastatin. At that time, MRI and blood work revealed no evidence of a stroke or elevation in his creatine kinase (CK) level. He stopped atorvastatin, and within 1 week the dysarthria resolved. During the next 8 months, he tried three other statins (lovastatin, pravastatin, and simvastatin). With each statin, the dysarthria returned in~1 week and resolved after stopping the medication. There was no elevation in his CK after the use of any of the statins. When he sought treatment in our medical center, he had experienced several weeks of dysarthria despite avoiding statin therapy for the previous 4 months. The dysarthria was worse in the evening and after prolonged periods of talking.On examination, he was markedly dysarthric. He had normal tongue movements and was not hypophonic. No cranial nerve abnormalities or proximal muscle weakness was detected. Repetitive nerve stimulation abnormalities were consistent with MG. The facial nerve showed a 50% decrement at baseline and Ͼ50% decrement at 30, 60, 120, and 180 seconds postexercise. The ulnar nerve showed a 6 to 7% decrement, and the spinal accessory nerve showed a 10 to 12% decrement postexercise. His acetylcholine receptor antibody level was Ͼ7.5 nmol/L (normal, Ͻ0.4 nmol/L). EMG did not reveal a myopathy, and CT of the chest did not show a thymoma. He was started on pyridostigmine (60 mg TID) and experienced rapid improvement in his speech.Discussion. To our knowledge, the only report in the literature associating statin use with worsening myasthenic symptoms involved a patient who developed ocular and systemic weakness on four separate occasions: three times with statins and once with a fibrate. 2 However, it is not clear that this patient had MG because no laboratory testing verified the diagnosis. 3 Our patient's history, repetitive nerve stimulation results, acetylcholine receptor antibody levels, and response to pyridostigmine substantiate the diagnosis of MG. It appears likely that statin use exacerbated his symptoms, given that dysarthria occurred on four separate occasions after four different statins, and each time he improved after discontinuation of the medication.Medications that exacerbate MG are thought to interrupt tr...

Myasthenia gravis exacerbation and diarrhea associated with erythromycin treatment

“…In severe case, respiratory difficulty can be seen and this can be a fatal condition in acute medicine. Several drugs are listed and reported as cause of exacerbation of MG. Those common drugs are antilipemic drug, steroid and antibiotic [5,6]. Antibiotic is a group of common drugs used at present.…”

More evidence for the association between statins and myasthenia gravis

“…In 2004, Cartwright et al 2 reported a patient with MG associated with statin use. Their patient, a 55-year-old man without prior history of myasthenia, developed recurrent dysarthria upon statin use.…”

“…Although statins are believed not to interfere with neuromuscular junction physiology, possible mitochondrial dysfunction on the mitochondria-rich preand postsynaptic interfaces of the motor end-plate could impair transmission in the neuromuscular junction and thus worsen myasthenic weakness. 2 It is also possible that some MG patients develop a statin-induced myopathy that leads to exacerbation of weakness. A relationship between statin-induced myopathy and immune-mediated disease was recently suggested in an abstract presented at the 2008 meeting of the American Academy of Neurology (Katzberg H, Miller RG, Grable P, Srinivasan J, Greenberg SA, Katz J, Amato A: "A necrotizing myopathy associated with statin use is responsive to immunomodulatory agents," Poster P02.131, 60th Annual Meeeting of the American Academy of Neurology, April 2008).…”

Lipidsenker- und andere toxische Myopathien

“…Im ei ge nen Pa ti en ten gut konn te nur in ei nem sehr ge rin gen Teil die ser Pa ti en ten eine addi ti ve neu ro mus ku lä re Er kran kung nachge wie sen wer den, die aber im mer dif feren zi al di ag nos tisch ab zu klä ren ist. In Einzel fäl len wur den un ter Sta ti nen auch Derma to myo si tis und Po ly myo si tis ähn li che Symp to me, die Ex azer ba ti on ei ner Myasthe nia gra vis und pe ri phe re Neu ro pa thien be schrie ben [14,15,16,17,18,19,20].…”