Myopathies are not an unusual complication of drug therapy. The major symptoms in drug-induced myopathies are proximal muscle weakness, increased muscle enzyme levels, electromyographic changes and histological lesions. Some drug-induced myopathies are associated with neuropathy. Drug-induced myopathies can be classified according to the presence or absence of muscular pain and associated neuropathy. Among painless myopathies, we can distinguish myopathies without neuropathy (corticosteroids), myopathies with neuropathy (colchicine, chloroquine and hydroxychloroquine) and myasthenic syndromes (D-penicillamine, antibiotics, beta-blockers). Among painful myopathies, the classification is similar: painful myopathies may or may not be associated with neuropathies. Painful myopathies include polymyositis (D-penicillamine, cimetidine, zidovudine) and other myopathies without polymyositis (clofibrate, statines, cyclosporin). Among the painful neuromyopathies, eosinophilia-myalgia syndrome is a recently described disorder associated with the use of L-tryptophan. Combinations of drugs (for example, a fibrate and a statine or cyclosporin and colchicine) can induce severe myopathies. If such drugs are used together a vigorous surveillance to detect any sign of myopathy is warranted. Instead of classifying drug-induced myopathies according to clinical features, a histological classification can be proposed. Many drugs can induce vacuolar myopathy (colchicine, chloroquine, amiodarone, cyclosporin, drugs causing hypokalaemia and lipid-lowering agents), some others cause a mitochondrial myopathy (zidovudine) or a necrotizing myopathy as seen with vincristine. Overall, several criteria for reporting drug-induced myopathy can be recommended: lack of pre-existent muscular symptoms, a free period between the beginning of the treatment and the appearance of symptoms, lack of another cause accounting for the myopathy, and complete or incomplete resolution after withdrawal of the treatment. Rechallenge of the treatment is not advisable because of the risk of a serious relapse. The exact mechanisms by which drugs cause myopathies are unknown. Some cases may be due to metabolic changes, whereas others may be immune mediated. Nevertheless, the aspect these conditions have in common is the regression of the myopathy with the discontinuation of the drug.

Drug-induced myopathies

Background: Renal failure is a recognized, but infrequent, complication following cardiac surgery. The causes for this condition are multifactorial, and a major concern is that the occurrence of postoperative acute renal failure is still associated with a high mortality rate.Methods and Materials: We report unexpected acute renal failure occurring in 4 patients after uncomplicated cardiac surgery. Each patient was taking a fibric acid derivative at the time of surgery. Renal failure occurred rapidly within 3 days of surgery and was associated with increased concentrations of skeletal muscle-derived creatine kinase (CK). One patient devel oped myoglobinuria, and another developed a malignant hyperthermia-like syndrome.Conclusions: These cases show that patients receiving lipid lowering medications could be at higher risk of developing acute renal failure after cardiac surgery. This association merits careful evaluation in large prospective studies and, if proved, would suggest that patients taking either s...

Acute renal failure after cardiopulmonary bypass: a possible association with drugs of the fibrate group.

Does hypothyroidism potentialize muscular toxicity of fibrates

Resume Un homme de 65 ans est explore en raison de l'apparition de myalgies et d'un deficit de la force musculaire. Le dosage des creatine-phosphokinases est 35 fois superieur a la valeur normale. L'electromyogramme est de type myogene diffus. La biopsie musculaire montre l'association de lesions necrotiques des fibres musculaires et d'un infiltrat mononuclee a disposition perivasculaire, faisant porter le diagnostic de polymyosite. Ce patient etait traite par fenofibrate depuis 10 ans en raison d'une hyperlipidemie. La posologie quotidienne etait de 600 milligrammes depuis 32 mois. Huit jours apres l'arret du fenofibrate, les anomalies cliniques et biologiques disparaissent. Une epreuve de reintroduction pratiquee 6 semaines plus tard provoque rapidement une ascension des creatine-phosphokinases a 43 fois la valeur normale. L'arret du fenofibrate entraine une guerison rapide et definitive. Le fenofibrate doit etre ajoute a la liste des drogues responsables de polymyosite iatrogene.

Polymyosite induite par le fénofibrate

Toxicité musculaire du fénofibrate

Muscular toxicity caused by fenofibrate

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Toxicité musculaire du fénofibrate

Muscular toxicity caused by fenofibrate