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HMG-CoA Reductase Inhibitors Clinical Features
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Statin agents inhibit 3-HMG-CoA reductase, the rate controlling enzyme in cholesterol synthesis (Fig 32 1) Adverse side effects including asymptomatic hyper-CKemia, myalgias, proximal weakness, and, less commonly, myoglobinuria occur with all of the major HMGCoA reductase inhibitors: lovastatin,12,15,17,18,31,36,37 simvastatin,11,13,14,37,38 provastatin,16,37 atorvastatin,10,37,39 uvastatin,37 and cerivastatin37,40,41 The nomenclature regarding statin-induced toxic myopathies in the published literature is unfortunately quite unsatisfactory, listing myalgias, myositis, and myopathy as three independent types of muscle disorders caused by statin use, when in fact the de nitions of these three subtypes may just re ect the spectrum of severity of the myopathy42 44 Reviews discussing statin myopathies cite a 2 7% incidence of myalgias and 01 10% incidence of weakness or elevated CK, and myoglobinuria developing in <05% of patients1,42,45,46 The National Heart Lung and Blood Institute advisory panel estimated the incidence of severe myopathy to be approximately 008% for lovastatin, simvastatin, and pravastatin43 The risk of toxic myopathy increases with the concomitant use of bric acids,17,18,26,30,31,39 niacin,31 erythromycin,47 cyclosporine,17,18 and ezetimibe,32 35 as do renal insuf ciency, and hepatobiliary dysfunction In this regard, 5% of patients taking both lovastatin and gem brozil developed a severe myopathy,26 while a severe myopathy complicated as many as 30% of patients receiving both lovastatin and cyclosporine12,17,18 Although the term myositis has been used to denote cases associated with markedly elevated serum CK levels, histopathological con rmation is lacking in most cases Myositis denotes an autoimmune attack on muscle Rare cases of myositis, particularly dermatomyositis, have been described in association with statin use16,48 55 An immune-mediated necrotizing myopathy may rarely develop in the setting of statin use In some cases the weakness continued to progress for 6 month or more after discontinuation of the statin and only improved once the patients were treated with immunosuppressive agents Whether the statins in such cases were
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NECROTIZING MYOPATHIES
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A number of drugs can cause a generalized necrotizing myopathy Affected individuals may complain of myalgias or weakness or they might just have asymptomatic elevations of their serum creatine kinase (CK) levels Severe necrotizing myopathy may be complicated by myoglobinuria and renal failure The degree of serum CK elevation is proportionate to the amount of muscle damaged
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Cholesterol-lowering medications including 3-hydroxy3methyl-glutaryl-coenzyme A (3-HMG-CoA) reductase inhibitors,10 18 bric acid derivatives,15,19 29 niacin,30,31 and ezetimibe32 35 can cause a toxic myopathy Most patients just have mild elevations in serum CK without any symptoms Others have myalgias and less frequently weakness Myoglobinuria is a rare event but can be complicated by death With discontinuation of the offending agent, the myalgias, weakness, and elevated serum CK levels tend to completely resolve but it may take several days to months However, rarely these agents may trigger an immune-mediated in ammatory myopathy, usually necrotizing, that requires treatment with immunosuppressive medications
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TABLE 32 1 TOXIC MYOPATHIES
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Pathogenic Classi cation Necrotizing myopathy
Drug Cholesterol-lowering agents Cyclosporine Labetolol Propofol Alcohol
Clinical Features Acute or insidious onset Proximal weakness Myalgias
Laboratory Features Elevated serum CK EMG: bs, PSWs, myotonia (statins, cyclosporine), and myopathic MUAPs
Histopathology Many necrotic muscle bers No evidence of endomysial in ammatory cell in ltrate invading non-necrotic muscle bers Autophagic vacuoles and inclusions are apparent in some muscle bers and in Schwann cells
Amphiphilic
Chloroquine Hydroxylchloroquine Amiodarone
Antimicrotubular Colchicine Vincristine
Acute or insidious onset Proximal and distal weakness Myalgias Sensorimotor neuropathy Hypothyroid (amiodarone) Acute or insidious onset Proximal and distal weakness Myalgias Sensorimotor neuropathy Acute or insidious onset Proximal weakness Myalgias Rhabdomyolysis Painful sensory neuropathy
Elevated serum CK EMG: bs, PSWs, myotonia (choroquine), and myopathic MUAPs NCS: axonal sensorimotor neuropathy Normal or elevated CK EMG: bs, PSWs, Myotonia (colchicine), and myopathic MUAPs NCS: axonal sensorimotor neuropathy Normal or elevated CK EMG: normal or myopathic NCS: axonal sensory neuropathy/ neuronopathy
Autophagic vacuoles and inclusions are evident in some muscle bers; nerve biopsies demonstrate axonal degeneration Muscle biopsies reveal ragged red bers, COX-negative bers May also see in ammatory cell in ltrates, cytoplasmic bodies, and nemaline rods Perivascular, perimysial, or endomysial in ammatory cell in ltrates
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