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Drugs causing myositis (by mechanism)
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- Drugs causing myopathy (painful vs. painless)
- Chronic Alcohol Myopathy
- High-dose steroids
- Colchicines
Drugs causing myositis (by mechanism)Inflammatory L-dopa, procainamide, cimetidine, D-penicillamine, L-tryptophan,
cholesterol-lowering agents, chloroquine, colchicine, emetine, aminocaproic acid, labetalol, cyclosporine and tacrolimus, isoretinoic acid (vitamin A analog), vincristine, alcohol Rhabdomyolysis and myoglobinuria cholesterol-lowering drugs, alcohol, heroin, amphetamine, toluene, cocaine, aminocaproic acid, pentazocine, phencyclidine Malignant hyperthermia halothane, ethylene, diethyl ether, methoxyflurane, ethyl chloride, trichloroethylene, gallamine, succinylcholine Mitochondrial Zidovudine (AZT) Myotonia 2,4- d-chlorophenoxyacetic acid, anthracene-9-carboxycyclic acid, cholesterol-lowering drugs, chloroquine, cyclosporine Myosin loss non-depolarizing neuromuscular blocking agents, IV steroids Drugs causing myopathy (painful vs. painless)Painless Alcohol (chronic), steroids Myoglobinuria CNS depressants, CNS stimulants, CO, cyanide, arsenic, snake venom Hypokalemia Diuretics, laxatives, licorice, carbenoxolone, ampho B, toluene, alcohol Painful Inflammatory Procainamide, phenytoin, levodopa, interferon alpha, cimetidine, leuprolide, PTU, penicillamine Mitochondrial AZT, germanium Drugs of abuse Alcohol, cocaine, heroin, PCP, volatile chemicals
IM injections, IVDA, cephalothin, lidocaine, diazepam, pethidine, pentazocine, meperidine, antibiotics in children Other Alcohol (acute), NMJ blockers (vecuronium, pancuronium), lovastatin < simvastatin, clofibrate, gemfibrozil, aminocaproic acid, excess vitamin E, etritinate, ipecac, emetine (overuse), organophosphates (acute poisoning), toxic oil syndrome, eosinophilia myalgias syndrome, snake venom (peak at 24-48 hrs) Chronic Alcohol MyopathyPainless, progressive proximal muscle weakness / ½ of alcoholics / damage is cumulative, but strength often restored after cessation Histology: type 2b fiber atrophy, no necrosis Acute Alcohol MyopathyWeak, painful, swollen muscles and cramps / may be limited to only one limb or muscle in most cases, cramps resolve in 1-2 days, pain and swelling takes 1-2 weeks, strength normal in 10-14 days / can develop rhabdomyolysis / lag time between alcohol consumption and elevated CK (several indirect mechanisms proposed) Labs: CK, LDH, myoglobin elevated Histology: necrosis and myofibrillar disorganization (inflammation is debatable) Hypokalemia Severe, painless proximal muscle weakness (no cramps, no swelling) / develops over hours/days / serum K between 1.4 – 2.5 / can cause rhabdomyolysis / complete reversal with K replacement Labs: CK, AST, aldolase elevated Histology: vacuolar changes, macrophages, +/- necrosis, regeneration Steroids (esp. dexamethasone, triamcinolone) Symmetrical, proximal muscle weakness / lower > upper / occasionally myalgias / may have generalized weakness, atrophy (severe cases) / very unlikely with < 10 mg/day or alternate day dosing Chronic Steroids Usually > 3 weeks / usually with other stigmata of steroids use Labs: CK usually normal / EMG shows normal rest activity, short-duration, low-amplitude motor units / Histology: type II atrophy, increased glycogen in type II fibers, lipid droplets in Type I fibers / EM shows sarcolemmal projections, vesicular bodies High-dose steroidsCan occur 1-2 days after treatment / often seen when treating severe asthma / may be generalized / may involve respiratory muscles / additional risk factors such as NMJ blockers, sepsis / near total recovery in weeks Histology: changes in both fiber types, vacuolar changes, regenerating fibers / normal EMG Licorice, carbenoxolone Pseudo-hyperaldosteronism / Na retention, edema, hypokalemia Chloroquine Usually starts in legs / takes 6 months to occur / may also have neuropathy EMG shows fibrillations, positive waves, occasionally myotonic discharges Histology: degeneration and acid phosphatase positive vacuoles in up to 50% of fibers / type I fibers predominantly affected / EM shows myeloid bodies and curvilinear bodies similar to neuronal ceroid lipofuscinosis Hydroxychloroquine (Plaquenil) is supposed to be safer, but I suspect the findings are similar Amiodarone may occur as early as 1 month / also get peripheral neuropathy, tremor, ataxia Perhexilene Anti-anginal agent / myopathy usually with long-term use only (reported as soon as 2 weeks, associated with rash, resolved with discontinuation Other side effects include weight loss, hypoglycemia, hepatic dysfunction, peripheral neuropathy
Note: sometimes misdiagnosed for polymyositis Sensory or motor nerve conduction is low-amplitude or absent
Histology: vacuolar myopathy Vincristine Histology: segmental necrosis, phagocytosis, spheromembranous degeneration / probably can have myopathy without neuropathy Zidovudine (AZT) Mechanism: ?false substrate for mitochondrial DNA polymerase Dose-related proximal muscle weakness and myalgias with pronounced wasting / elevated CK / usually improves with discontinuation Histology: ragged RED fibers / rod-body formation, necrosis, microvacuolization / EM has various changes Cannot always distinguish from HIV myositis
Rapidly progressive, necrotizing myopathy / weakness, myalgias, CK 8000-30,000 / can lead to rhabdomyolysis / incidence of 0.5% (compare to incidence of elevated LFT of 2%) / risk increased with combination of lovastatin, gemfibrozil, niacin, immunosuppressive agents Histology: necrosis Much less common with Simvastatin Aminocaproic acid usu. > 4 wks, can occur as early as several days Etritinate (dermatology drug) mild-transient myalgias occur in 15%, do not require discontinuation / occasionally, can be more severe Synovial fluid analysis
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