53 – Alcoholic Myopathy: Clinical Aspects

This chapter describes the clinical aspects of alcoholic myopathy. Ethanol consumption may cause acute and chronic deleterious effect on skeletal muscle, inducing muscle weakness, atrophy, and myocyte death. Acute myopathy has and sporadic presentation among binge consumers. Chronic alcoholic myopathy has a prevalence of 40–60% in a population of alcohol misusers. Muscle weakness, myalgia and swelling are the main features of acute myopathy. In chronic myopathy, the most relevant features are proximal progressive muscle weakness and atrophy. There are more subclinical cases, which can be detected evaluating muscle weakness by myometry. Skeletal muscle involvement in alcoholism is related to other systemic diseases—such as dilated cardiomyopathy, peripheral neuropathy, malnutrition and liver cirrhosis. Myocytolysis and Type II fiber atrophy are the most prominent features in alcoholic myopathy. Because of the lack of a specific histological pattern, the diagnosis of alcoholic myopathy requires a characteristic clinical pattern and careful exclusion of other causes of myopathy. The physiopathological mechanisms that determine the muscle damage induced by ethanol are still not completely understood. Studies have shown that ethanol has a toxic direct effect, that is, producing muscle damage by altering membrane fluidity, channels, pumps and ionic transients, depression of muscle contractility, and protein synthesis or mitochondrial function.