This article includes discussion of alcoholic myopathy, acute alcoholic myopathy, alcoholic rhabdomyolysis, alcoholic myoglobinuria, acute alcoholic myopathy, and chronic alcoholic myopathy. The foregoing terms may include synonyms, similar disorders, variations in usage, and abbreviations.
Alcohol can produce several myopathic disorders, including acute alcoholic myopathy with or without myoglobinuria, hypokalemic myopathy, chronic atrophic myopathy, and cardiomyopathy (Perkoff 1971; Martin et al 1985; Victor 1986; Kuncl and Wiggins 1988; Lanska and Ruff 1993). Acute alcoholic myopathy (also termed alcoholic rhabdomyolysis and acute alcoholic necrotizing myopathy) is an uncommon syndrome of abrupt muscle injury that typically occurs in malnourished chronic alcoholics following a binge or in the first days of alcohol withdrawal; experimental studies have demonstrated that both alcohol and nutritional factors are necessary to produce this syndrome (Baruah et al 1988; Kuncl and Wiggins 1988; Lanska and Ruff 1993). Severity ranges from asymptomatic transient elevation of creatine kinase to frank rhabdomyolysis with myoglobinuria. Although in most instances full recovery occurs within days to weeks, death may occur in the setting of acute renal failure and hyperkalemia. Chronic alcoholic myopathy is a gradually evolving syndrome of proximal weakness, atrophy, and gait disturbance that frequently complicates years of alcohol abuse. Muscle strength correlates with lifetime consumption of ethanol. Recovery occurs if alcohol is avoided, but the timeframe of improvement is weeks to months, in contrast to the rapid recovery typical of acute alcoholic myopathy. Pathogenic mechanisms include impaired gene expression and protein synthesis as well as increased oxidative damage and apoptosis.
• Acute alcoholic myopathy develops suddenly in the context of binge drinking and is characterized by painful muscle weakness and myonecrosis.
• Chronic alcoholic myopathy develops gradually and is characterized by painless weakness of proximal muscles.
• Recovery occurs if alcohol is avoided, but the time to recovery varies from rapid (days to weeks) with the acute form to protracted (weeks to months) with the chronic form.
Historical note and terminology
In 1822, American physician James Jackson (1777-1867) concluded that neuropathic lesions could not explain all of the signs in alcoholics and suggested that that their muscles were also abnormal (Jackson 1822).Ekbom et al 1964). muscle disease (Dreschfield 1885; Hun 1885). Several pathologic reports appeared in the late 19th century, particularly in Germany (Oh 1972).
Modern recognition of the link between alcohol abuse and myopathy and the differentiation of acute and chronic alcoholic muscle disorders dates to the 1950s and 1960s, particularly by Swedish investigators Ragnar Hed and Karl Ekbom (Hed et al 1955; Hed et al 1962; Fahlgren et al 1957; Ekbom et al 1964). These investigators described 2 major syndromes: (1) acute alcoholic myopathy in which myonecrosis develops suddenly in the context of binge drinking; and (2) chronic alcoholic myopathy in which weakness of proximal muscles develops gradually. In addition, alcoholic individuals without muscle-related symptoms were found to have electromyographic and histologic evidence of myopathy (Ekbom et al 1964). In the late 1960s American internist George Thomas Perkoff (1926-2012) and colleagues at Washington University School of Medicine in St. Louis described individuals with chronic alcohol abuse who developed an acute reversible muscular syndrome with dramatic muscle cramps, tender muscles, weakness, variable myoglobinuria, increased creatine kinase blood levels, and a reduced ability to increase serum lactic acid levels in response to ischemic exercise (Perkoff et al 1966; Perkoff et al 1967). Subsequent studies have linked alcoholic myopathy directly to injurious effects of ethanol and acetaldehyde (Song and Rubin 1972). The molecular basis of the myopathic effects of alcohol has remained elusive.
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