Sporadic rippling muscle disease unmasked by simvastatin

Baker, Steven K.; Tarnopolsky, Mark A.

doi:10.1002/mus.20575

Cited by 27 publications

(19 citation statements)

References 29 publications

(57 reference statements)

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“…It is unclear whether these syndromes are induced or unmasked by statins. However, there have been reports of a case each for rippling myopathy, myotonic dystrophy, Kennedy disease, McArdle disease, and acid maltase deficiency, which were clearly unmasked by statins 1,16,19. In the case of rippling myopathy, transient seropositive generalized MG was documented 1 year after onset of the rippling myopathy 1…”

Section: Discussionmentioning

confidence: 99%

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Statins may aggravate myasthenia gravis

Dhall

Young

et al. 2008

Muscle and Nerve

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Statin-induced myopathy is well-known, but the effect of cholesterol-lowering agents on myasthenia gravis (MG) has not been studied in detail. We investigated statin use and its effects on MG among patients with this disease. Statin information was systemically obtained from 170 patients being treated at the Neuromuscular Disease Clinic at the University of Alabama at Birmingham. When a new myalgic syndrome or worsening of MG developed within 4 months after statin treatment, no other likely cause was found, and clinical improvement occurred either with or without discontinuation of the statin, we considered these symptoms to be statin-induced. Fifty-four patients (31%) were on statins. The statin group had proportionally more males, and older patients compared with the non-statin group. A myalgic syndrome was noted in 7 (13%) patients, but it resolved without any sequelae after withdrawal of the statin. MG worsening occurred in 6 (11%) patients without regard to type of MG or brand of statin. MG worsening occurred independently of myalgic syndrome and involved predominantly oculobulbar symptoms within 1-16 weeks of statin treatment. In 4 patients, additional treatment was needed to reverse MG worsening. Statins are safe in the majority of MG patients, but their use must be accompanied by close observation for possible MG worsening.

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Section: Discussionmentioning

confidence: 99%

“…Their side effects on muscle are well known and range from myalgia and muscle cramp to elevation of creatine kinase (CK), myopathy, and rhabdodomyolysis 13,17. It is also known that statins may unmask underlying neuromuscular diseases 1,16,19. There have been a few case reports of worsening of myasthenia gravis (MG) in patients treated with statins 3,9,12.…”

mentioning

confidence: 99%

Statins may aggravate myasthenia gravis

Dhall

Young

et al. 2008

Muscle and Nerve

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“…An incompletely mapped defect on chromosome 1q41 and multiple missense mutations in the caveolin-3 gene cause autosomal dominant RMD1 and 2 respectively [107][108]. A report of previously undiagnosed RMD presenting in a fiftyfour year-old patient treated with statins suggested that symptoms resolved with discontinuation of simvastatin but reoccurred on statin rechallenge [109].…”

Section: Rippling Muscle Disease (Rmd)mentioning

confidence: 98%

Role of Genetic Factors in Statins Side-Effects

Scarpini

Cappellone²,

Auteri³

et al. 2012

CHDDT

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Statins are relevant drugs involved in the reduction of cardiovascular events both in primary and secondary prevention. Related muscular side-effects are the most common cause of withdrawal and statins discontinuation could induce a negative rebound effect in terms of vascular events. Among factors in association with statins side-effects the combination with other drugs and the female sex are established conditions. However recent data suggest a specific genetic influence in intolerance development, at least for some statins. Indeed a genome-wide study in patients treated with simvastatin found an impressive association between single-nucleotide polymorphisms (SNPs) located within SLCO1B1 gene on chromosome 12 and established myopathy. Furthermore, the association between the SLCO1B1*5 variant and side-effects was found also in patients treated with atorvastatin but not, apparently, with pravastatin and categorized as carriers of mild-myopathy. Recently a similar evidence has been suggested in type 2 diabetic patients treated mainly with simvastatin. However another relevant issue is that, apart from genetic influence in liver transporters influencing drug levels, the complexity of mechanisms involved in the muscular side effects of statins has been addressed by the evidence of other influencing pathways such as the variant within the COQ2 gene involved in Coenzyme Q(10) mild-asymptomatic deficiency and skeletal muscle drug transporters expression. In conclusion, the picture of putative pharmacogenetic modulation of statins safety is reaching a growing body of evidence for translation into clinical practice but more specific studies for each single statin, in different clinical settings, both from genome-wide or competitive candidate genes evaluation, are needed before describing a definitive class-risk profile.

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“…Acquired or immuno-mediated RMD is associated with myasthenia gravis. This association was first described in 1996 and in the last decade a small number of case reports followed (Table 1) [2][3][4][5][6][7]. Immuno-mediated RMD is clinically indistinguishable from hereditary RMD.…”

mentioning

confidence: 92%