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Drug-induced myopathies

Author
Marc L Miller, MD
Section Editors
Ira N Targoff, MD
Jeremy M Shefner, MD, PhD
Deputy Editor
Monica Ramirez Curtis, MD, MPH

INTRODUCTION

Although the precise incidence is unknown, drug-induced myopathy is among the most common causes of muscle disease. Drug-induced myopathy ranges from mild myalgias with or without mild weakness to chronic myopathy with severe weakness and to massive rhabdomyolysis with acute renal failure [1,2]. Over 150 agents have been associated with rhabdomyolysis [3]. This topic will review drug-induced myopathies. Rhabdomyolysis and statin myopathy are discussed in detail separately. (See "Causes of rhabdomyolysis" and "Clinical manifestations and diagnosis of rhabdomyolysis" and "Statin myopathy".)

MECHANISMS

Drug-induced myopathy may result from several different mechanisms [4,5]:

Direct myotoxicity – Examples include alcohol, cocaine, glucocorticoids, lipid-lowering drugs, antimalarials (which are associated with vacuolar myopathies), colchicine (which is associated with vacuolar myopathies), and zidovudine (which causes a mitochondrial myopathy).

Immunologically induced inflammatory myopathy – The myopathy associated with D-penicillamine is an example of this mechanism.

Indirect muscle damage – This problem can occur by a variety of mechanisms including drug-induced coma with subsequent ischemic muscle compression, drug-induced hypokalemia (eg, diuretics), drug-induced hyperkinetic states (eg, delirium tremens or seizures secondary to alcohol), dystonic states associated with phenothiazines, hyperthermia related to cocaine use, and the neuroleptic malignant syndrome.

                    

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Literature review current through: Nov 2016. | This topic last updated: Mon Oct 03 00:00:00 GMT 2016.
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