DRUG-INDUCED MYOPATHIES

DRUG-INDUCED MYOPATHIES is a topic covered in the Harrison's Manual of Medicine.

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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.

TABLE 198-2: Drug-Induced Myopathies
DRUGSMAJOR TOXIC REACTION

Lipid-lowering agents

 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.
GlucocorticoidsAcute, 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 agentsAcute quadriplegic myopathy can occur with or without concomitant glucocorticoids.
ZidovudineMitochondrial myopathy with ragged red fibers

Drugs of abuse

 Alcohol

 Amphetamines

 Cocaine

 Heroin

 Phencyclidine

 Meperidine

All drugs in this group can lead to widespread muscle breakdown, rhabdomyolysis, and myoglobinuria.

Local injections cause muscle necrosis, skin induration, and limb contractures.

Autoimmune myopathy

 Statins

 Checkpoint inhibitors

 D-Penicillamine

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

 Amiodarone

 Chloroquine

 Hydroxychloroquine

All amphophilic drugs have the potential to produce painless, proximal weakness associated with necrosis and autophagic vacuoles in the muscle biopsy.

Antimicrotubular drugs

 Colchicine

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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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.

TABLE 198-2: Drug-Induced Myopathies
DRUGSMAJOR TOXIC REACTION

Lipid-lowering agents

 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.
GlucocorticoidsAcute, 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 agentsAcute quadriplegic myopathy can occur with or without concomitant glucocorticoids.
ZidovudineMitochondrial myopathy with ragged red fibers

Drugs of abuse

 Alcohol

 Amphetamines

 Cocaine

 Heroin

 Phencyclidine

 Meperidine

All drugs in this group can lead to widespread muscle breakdown, rhabdomyolysis, and myoglobinuria.

Local injections cause muscle necrosis, skin induration, and limb contractures.

Autoimmune myopathy

 Statins

 Checkpoint inhibitors

 D-Penicillamine

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

 Amiodarone

 Chloroquine

 Hydroxychloroquine

All amphophilic drugs have the potential to produce painless, proximal weakness associated with necrosis and autophagic vacuoles in the muscle biopsy.

Antimicrotubular drugs

 Colchicine

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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