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Alcoholic skeletal myopathy, a clinical and pathological study
The Quarterly Journal of Medicine
|June 1, 1985
Summary
Chronic heavy alcohol intake frequently causes skeletal muscle disease, specifically type II muscle fibre atrophy. Abstinence from alcohol improves muscle function, suggesting ethanol
Area of Science:
- Neurology
- Toxicology
Background:
- Chronic heavy alcohol intake is prevalent.
- Alcohol's impact on skeletal muscle is not fully understood.
- Existing research often overlooks direct muscle toxicity.
Purpose of the Study:
- To investigate the prevalence and nature of skeletal muscle disease in chronic alcohol consumers.
- To determine if other alcohol-related conditions explain muscle abnormalities.
- To assess the effect of alcohol abstinence on muscle health.
Main Methods:
- Histological examination of quadriceps muscle biopsies from 151 inpatients with heavy alcohol intake history.
- Clinical assessment for symptoms, peripheral neuropathy, cirrhosis, and malnutrition.
- Serum creatine kinase activity measurement.
- Follow-up studies after alcohol abstinence.
Main Results:
- 60% of patients exhibited abnormal muscle biopsies, primarily type II muscle fibre atrophy.
- Acute myopathy and rhabdomyolysis were observed in a small percentage.
- Cirrhosis, malnutrition, and neuropathy did not fully explain muscle abnormalities.
- Serum creatine kinase was an insensitive marker for alcoholic myopathy.
- Alcohol abstinence led to consistent muscle function improvement, while continued use worsened atrophy.
Conclusions:
- Chronic skeletal myopathy is a common consequence of alcohol abuse.
- Ethanol likely exerts a direct toxic effect on muscle fibres.
- Muscle function recovery is possible with abstinence, independent of neuropathy recovery.