Drugs (including glucocorticoids and lipid-lowering agents) and toxins (e.g., alcohol) are associated with myopathies (Table 198-2). In most cases, weakness is symmetric and involves proximal limb girdle muscles; myalgia and cramps may also occur. An elevated CK is often found. Diagnosis often depends on resolution of signs and symptoms with removal of offending agent.
|DRUGS||MAJOR TOXIC REACTION|
HMG-CoA reductase inhibitors
Fibric acid derivatives
Niacin (nicotinic acid)
|Drugs belonging to all three of the major classes of lipid-lowering agents can produce a spectrum of toxicity: asymptomatic serum creatine kinase elevation, myalgias, exercise-induced pain, rhabdomyolysis, and myoglobinuria.|
|Glucocorticoids||Acute, high-dose glucocorticoid treatment can cause acute quadriplegic myopathy. These high doses of steroids are often combined with nondepolarizing neuromuscular blocking agents but the weakness can occur without their use. Chronic steroid administration produces predominantly proximal weakness.|
|Nondepolarizing neuromuscular blocking agents||Acute quadriplegic myopathy can occur with or without concomitant glucocorticoids.|
|Zidovudine||Mitochondrial myopathy with ragged red fibers|
Drugs of abuse
All drugs in this group can lead to widespread muscle breakdown, rhabdomyolysis, and myoglobinuria.
Local injections cause muscle necrosis, skin induration, and limb contractures.
|Use of statins may cause an immune-mediated necrotizing myopathy associated with HMG-CoA reductase antibodies. Check point inhibitors can be complicated by myositis, myasthenia gravis, and immune-mediated neuropathies. Myasthenia gravis has also been reported with penicillamine.|
Amphophilic cationic drugs
|All amphophilic drugs have the potential to produce painless, proximal weakness associated with necrosis and autophagic vacuoles in the muscle biopsy.|
|This drug produces painless, proximal weakness especially in the setting of renal failure. Muscle biopsy shows necrosis and fibers with autophagic vacuoles.|
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