Acute alcoholic myopathy is a syndrome of sudden muscle necrosis which occurs in the setting of binge drinking. The clinical expression of muscle injury ranges from an asymptomatic elevation in serum creatine kinase to fulminant rhabdomyolysis with muscle pain, swelling and myoglobinuria. Clinical and experimental studies suggest that this represents a 'toxic' myopathy; however, the cellular basis of the postulated myotoxic effect of ethanol is unknown. Chronic alcoholic myopathy is a more indolently evolving syndrome of proximal weakness and muscle atrophy which accompanies prolonged alcohol abuse. Type II muscle fiber atrophy, the major histologic feature of this disease, is also common in alcoholics without symptoms of muscle disease and supports the notion of a 'subclinical' chronic alcoholic myopathy. The possible contributions of ethanol, its metabolites, and the mineral and other nutritional deficiencies which frequently accompany ethanol abuse to the pathogenesis of this disorder remain to be determined. Management of these clinically and presumably pathogenically distinct muscle syndromes involves recognition of a compatible clinical presentation; exclusion of neuromuscular diseases which may mimic these syndromes; appropriate treatment of associated mineral or electrolyte imbalances, nutritional deficiency, or complicating renal disease; and a successful program to encourage abstinence from alcohol.
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