Alcoholic skeletal myopathy, a clinical and pathological study.
1985
SUMMARY One hundred and fifty-one inpatients with a history of chronic heavy alcohol intake were examined for evidence of muscle disease. Ninety-two patients (60 per cent) had histologically abnormal biopsies of the quadriceps muscle. The most common abnormality, which was often severe, was type II muscle fibre atrophy. Seven patients (5 per cent) had histological evidence of acute myopathy, one of whom presented with the full clinical picture of acute rhabdomyolysis.
Twenty-three patients had cirrhosis, 36 were significantly malnourished and 98 had evidence of a peripheral neuropathy. None of these features, however, were sufficient to account for the muscle abnormalities. There was no clear relationship between musculo-skeletal symptoms and muscle biopsy histology. Serum creatine kinase activity was elevated in only 23 subjects and was an insensitive indicator of subclinical acute myopathy and of chronic alcoholic myopathy.
Follow-up studies after abstinence from alcohol invariably showed both objective and subjective improvement of muscle function — often in the absence of any clinical recovery from the peripheral neuropathy. Continued alcohol consumption was accompanied by persistence and often deterioration of muscle fibre atrophy. It is concluded that chronic skeletal myopathy is a frequent consequence of alcohol abuse and may result from a direct toxic effect of ethanol on muscle fibres.
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