Clofibrate-lnduced acute muscular syndrome

Sekowski, Ignacy; Samuel, Paul

doi:10.1016/0002-9149(72)90053-7

Cited by 38 publications

(10 citation statements)

References 12 publications

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“…Similar enzyme changes have been observed in asymptomatic subjects (Langer and Levy, 1968). Other reports of myositis have since appeared (Sekowski and Samuel, 1972) and it appears to be especially prone to occur in nephrotic patients, perhaps related to their low serum albumin levels which lead to an increased amount of active drug in the plasma (Bridgman et al, 1972). Increased ventricular irritability thought to be due to clofibrate has been observed in one subject (La Rosa et al, 1969) .…”

Section: Side and Toxic Effectssupporting

confidence: 53%

Lipid Lowering Drugs and Hyperlipidaemia

Levy

Rifkind

1973

Drugs

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Section: Side and Toxic Effectssupporting

confidence: 53%

Lipid Lowering Drugs and Hyperlipidaemia

Levy

Rifkind

1973

Drugs

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“…These observations may also provide further insight into the pathogenesis of the muscular syndrome in patients who receive clofibrate therapy for treatment of hvperlipidemias (48,49). Our previous electromyographic and electron microscopic studies revealed the development of myotonia and dilation of transverse tubules of skeletal muscle fibers of rats similarly treated wvith clofibrate (50).…”

Section: Discussionmentioning

confidence: 61%

Leucine Oxidation and Protein Turnover in Clofibrate-induced Muscle Protein Degradation in Rats

Paul¹,

Adibi²

1980

J. Clin. Invest.

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A B S T R A C T Treatment of hvperlipidemia withclofibrate may result in development of a muscular svndrome. Our previous investigation (1979. J. ClitG. Ivce.st. 64: 405.) showed that chronic administration of clofibrate to rats causes mvotonia and decreases glucose and fatty acid oxidation and total protein of skeletal muscle. In the present experimiients we have investigated amino acid and protein metabolism in these rats. Clofibrate administratioin decreased the concenitration of all three branched-chain amino acids without affecting those of others in muscle. Studies to examine the mechanism of decreases in muscle concenitrationis of branched-chain amiiino acids showed the followiing: (a)

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“…Serial measurements of serum CPK were first proposed with clofibrate in 1972, following a case of "acute muscular syndrome" in 1968 [26]. Although CPK elevations may be a sensitive marker of muscle damage, they are not particularly predictive of patients at risk for developing myopathy.…”

Section: Myotoxicitymentioning

confidence: 99%

A general assessment of the safety of HMG CoA reductase inhibitors (statins)

Black¹

2002

Curr Atheroscler Rep

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Few principles in medicine today are as well accepted as the benefits of using statins to reduce cardiovascular risk factors and to prevent cardiovascular disease. The recent withdrawal of a statin (cerivastatin) has lead to a re-examination of all statins, and an attempt to better assess the risk-benefit ratio of this class of drugs. Although the benefits of statin treatment are well known from a myriad of clinical trials, the safety of these compounds has not been an issue since lovastatin was first introduced in 1987. This report provides a brief review of statin safety, and reiterates the excellent profile of this class of drugs.

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Clofibrate-lnduced acute muscular syndrome

Cited by 38 publications

References 12 publications

Lipid Lowering Drugs and Hyperlipidaemia

Lipid Lowering Drugs and Hyperlipidaemia

Leucine Oxidation and Protein Turnover in Clofibrate-induced Muscle Protein Degradation in Rats

A general assessment of the safety of HMG CoA reductase inhibitors (statins)

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