Cholesterol‐lowering agent myopathy (CLAM)

London, Scott F.; Gross, Karl F.; Ringel, Steven P.

doi:10.1212/wnl.41.7.1159

Cited by 51 publications

(31 citation statements)

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“…One of the most important factors for predicting risk of myopathy is also way of metabolization of statins. Most of them are metabolized by cytochrome P 450 family with the exception of pravastatin [39][40][41]. Lovastatin, simvastatin and atorvastatin are metabolized by cytochrome P 450 P3A like nifedipine, felodipine, amiodarone, macrolide antibiotics, cisapride, omeprazole etc.…”

Section: Risk Factors For Statins Toxicitymentioning

confidence: 99%

“…That is explanation why during treatment with pravastatin there were less muscle complications observed. The next explanation in favour of pravastatin is that it is hydrophilic statin in contrast to all other above named statins which is not causing "increased fluidity of muscle cell membranes" responsible for the increased risk of myopathy development [41]. Poor coenzyme Q10 status and antioxidant status in the body are also a predisposing factors for statin toxicity [18-20, 42, 43].…”

Section: Risk Factors For Statins Toxicitymentioning

confidence: 99%

“…A number of manifestations of muscle effects have been reported, with rhabdomyolysis the most feared. Adverse effects are dose dependent, and risk is amplified by drug interactions that functionally increase statin potency, often through inhibition of the cytochrome P450 3A4 system [40,41]. An array of additional risk factors for statin toxicity are those that amplify (or reflect) mitochondrial or metabolic vulnerability, such as metabolic syndrome factors, thyroid disease, and genetic mutations linked to mitochondrial dysfunction.…”

Section: Etiology and Mechanismsmentioning

confidence: 99%

“…Thus,it is not surprising that coenzyme Q10 concentrations are decreased during statin therapy due to both decrease of LDL cholesterol and inhibition of its synthesis. It was shown that during statin therapy significant decrease of coenzyme Q10 was observed (up to 40%) and subsequent disorder of mitochondrial energetic metabolism may lead to myopathy [41]. The reduction in serum coenzyme Q10 may be dose related and so may be the muscle damage [42].…”

Section: Possible Role Of Antioxidantsmentioning

confidence: 99%

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Clinical Manifestations of Adverse Effects of Statins, Oxidative Stress and Possible Role of Antioxidants in Prevention?

Fedačko¹,

Singh²,

Chaithiraphan³

et al. 2010

TONUTRAJ

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Abstract:Background: There is evidence that statins are potent and effective agents with several pleiotropic effects for treatment of coronary artery disease(CAD). Statin may have adverse effects, if given in higher doses and in combinations.Methods: Internet search till 2009 and discussion with colleagues.Results: Statins are wonder drugs influencing wide range of physiological, biochemical,and biological functions.This list appears to be quite large and includes hypolipidemic, vasodilative, antithrombotic, antioxidant, antiinflammatory, antiproliferative, anticoagulant, agiogenic and bone formation inducing functions. Myopathy is the most frequent side effect of statins and in some cases may have a form of severe rhabdomyolysis. Less common adverse effects include hepatotoxicity, peripheral neuropathy, impaired myocardial contractility and autoimmune diseases. Rare manifestations of statin intolerance may be; pulmonary, psychiatric, ophthalmic and amyotropic lateral sclerosis. The risk of these unfavorable effects is largely outweighed by great reduction of cardiovascular events in statin users. The spectrum of statin-related myopathy ranges from common but clinically benign myalgia to rare but life-threatening rhabdomyolysis. Observational studies suggest that myalgia can occur in up to 10% of persons prescribed statins, whereas rhabdomyolysis continues to be rare. The mechanisms of statin-related myopathy are unclear. The criteria of diagnosis of myopathy do not bother about the symptoms of patients and oxidative stress, in absence of raised muscle enzymes.Coenzyme Q10 and other antioxidants are not considered in the prophylaxis of statin toxicity. Because one study showed no decrease in CoQ in the muscle in presence of toxicity, although several studies indicate a reduction in serum levels. Conclusion:Statins would be used more commonly in near future due to their cholesterol lowering and antiinflammatory effects. There would be a marked increase in the Number of patients with statin toxicity. Several studies have reported a significant reduction in the serum CoQ in patients receiving statins.Such concern has also been expressed by the International College of Cardiology in their meeting in April 2002April and 2005April and 2009, proposing that coenzyme Q10 and other antioxidants should be considered in the prevention as well as treatment of statin intoxication.

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Section: Risk Factors For Statins Toxicitymentioning

confidence: 99%

Section: Risk Factors For Statins Toxicitymentioning

confidence: 99%

Section: Etiology and Mechanismsmentioning

confidence: 99%

Section: Possible Role Of Antioxidantsmentioning

confidence: 99%

See 2 more Smart Citations

Clinical Manifestations of Adverse Effects of Statins, Oxidative Stress and Possible Role of Antioxidants in Prevention?

Fedačko¹,

Singh²,

Chaithiraphan³

et al. 2010

TONUTRAJ

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“…The muscle disorder associated with them are coined cholesterol-lowering agents myopathy (CLAM) 1 . The annual incidence of rhabdomyolysis in patients taking statins is 3.4 per 100000 persons 2 .…”

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confidence: 99%

Myotonic potentials in statin-induced rhabdomyolysis

Almeida

Lissa

Melo

2008

Arq. Neuro-Psiquiatr.

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Lipid lowering drugs are used worldwide to control dyslipidemias. The muscle disorder associated with them are coined cholesterol-lowering agents myopathy (CLAM) 1 . The annual incidence of rhabdomyolysis in patients taking statins is 3.4 per 100000 persons 2 . Between 1987 and 2001 there were 42 deaths +related to statin-induced rhabdomyolysis, resulting in a mortality rate of 0.15 per million of prescriptions 3 . Although myotonic potentials have been described in some drug-related myopathies, they are rarely reported in CLAM. Though there are a few experimental myotonic myopathy associated with statin in rabbits 4-6 , there was only one single report describing 5 patients with this finding in humans 7 .We report a patient with statin-related rhabdomyolysis and profuse myotonic potentials in the needle EMG with clinical and electrophysiological recovery shortly after the statin interruption. CaSeA 68 year-old Asian Brazilian woman was admitted with progressive painless weakness for one week, started on the proximal muscles of the four limbs and neck flexors with rapid progression to inability to walk and elevate the limbs. Urine was redbrown in color. Thirty days before the admission she was put on simvastatin due to hypercholesterolemia. Other medication she was taking was enalapril for mild hypertension. There was no personal or family history of myopathy. On neurological examination, abnormal findings were grade 2 (MRC) strength in the proximal lower limb muscles and grade 3 in the proximal upper limb muscles, grade 4 in the distal muscles and hypoactive deep tendon reflexes. No clinical myotonia was detected.A complete blood count, electrolytes, creatinine, glucose, TSH, and free T4 were all normals. Myoglobin was detected in the urine. CPK was 22.260 U/l on the admission day and 55.000 U/l on the third day. AST and ALT were 790 and 750 U/l, respectively. The nerve conduction studies perfomed in both arms and legs showed normal results in the median, ulnar, superficial radial, tibial, peroneal, superficial peroneal and sural nerves bilaterally. The F wave latencies were normal in the median, ulnar, fibular and tibial nerves bilaterally. The needle EMG perfomed with disposable monopolar needle in cervical paraspinal, supraspinatus, deltoid, triceps, abdutor pollicis brevis and first dorsal interosseus in the upper right limb and tibialis anterior, gastrocnemius, vastus lateralis and iliopsoas in the right lower limb showed rare positive sharp waves and fibrillations in the right supraspinatus muscle, as well as a few small amplitude and short duration (SASD) motor unit potentials (MUP) in the right iliopsoas muscle. On the other hand, the needle study showed profuse amount of myotonic potentials in deltoid, supraspinatus, iliopsoas and cervical paraspinal muscles on the right side (Fig 1).Simvastatin was stopped and vigorous hydration was started to prevent acute renal failure. She was discharged two weeks later with normal strength, renal function and CPK levels. A second needle EMG performed 30 days after...

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