2008
DOI: 10.1007/s11910-008-0011-4
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Statin myopathy

Abstract: Many different classes of medications can cause toxic myopathy. One of the most frequently implicated classes is the statins. Statin myotoxicity ranges from asymptomatic creatine kinase elevations or myalgias to muscle necrosis and fatal rhabdomyolysis. Statins may also cause an autoimmune myopathy requiring immunosuppressive treatment. The mechanisms of statin myotoxicity are unclear. If unrecognized in its early manifestations, complications from continued statin therapy may lead to rhabdomyolysis and death.… Show more

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Cited by 33 publications
(34 citation statements)
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“…These effects result from impaired protein prenylation, deficiency of coenzyme Q involved in mitochondrial electron transport, genetic varia-*Address correspondence to this author at the Halberg Hospital and Research Institute, Civil Lines, Moradabad-10(UP)244001, India; Tel/Fax: 0091 591 2417437; E-mail: icn2005@sancharnet.in tions and antioxidant protection, abnormal protein glycosylation due to dolichol shortage, or deficiency of selenoproteins [1][2][3][4][5][6][7]. Statins inhibit 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol biosynthesis, which converts HMG-CoA to mevalonate.…”
Section: Introductionmentioning
confidence: 99%
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“…These effects result from impaired protein prenylation, deficiency of coenzyme Q involved in mitochondrial electron transport, genetic varia-*Address correspondence to this author at the Halberg Hospital and Research Institute, Civil Lines, Moradabad-10(UP)244001, India; Tel/Fax: 0091 591 2417437; E-mail: icn2005@sancharnet.in tions and antioxidant protection, abnormal protein glycosylation due to dolichol shortage, or deficiency of selenoproteins [1][2][3][4][5][6][7]. Statins inhibit 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol biosynthesis, which converts HMG-CoA to mevalonate.…”
Section: Introductionmentioning
confidence: 99%
“…Statins inhibit 3-hydroxy-3-methylglutarylcoenzyme A (HMG-CoA) reductase, the rate-limiting enzyme in cholesterol biosynthesis, which converts HMG-CoA to mevalonate. Statins lower plasma low-density lipoprotein (LDL) cholesterol by causing intracellular cholesterol depletion and upregulating the expression of LDL receptors [4][5][6][7]. Apart from cholesterol, mevalonate is also the substrate for the synthesis of nonsteroid isoprenoids including farnesylpy-rophosphate, geranylgeranylpyrophosphate (both attached to small GTP-binding proteins by protein prenyltransferases), coenzyme Q, dolichol, isopentenyladenosine, etc.…”
Section: Introductionmentioning
confidence: 99%
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“…On the other hand, adverse effects of statins could have serious impact and form a significant barrier to therapy adherence. A variety of muscle-related side effects could occur [3][4].…”
Section: Introductionmentioning
confidence: 99%
“…Myopathy may be defined by a ten-fold elevation in creatine kinase (CK) with muscle pain or weakness, while rhabdomyolysis is usually associated with CK >10,000 international units per litre (IU/l) and acute kidney injury, which may be lifethreatening. [1][2][3][4][5][6][7][8] The placebo-corrected incidence of rhabdomyolysis in a systematic review of 20 statin trials was 1.6/100,000 per year, 9 but the incidence is likely to be higher than this in everyday clinical practice when statins are knowingly or inadvertently co-prescribed with drugs that inhibit their metabolism. 10 Against this background we wish to report a case of rhabdomyolysis that occurred when fusidic acid was co-prescribed with atorvastatin, potentiating the toxicity of both drugs.…”
Section: Introductionmentioning
confidence: 99%