ALCOHOLIC MUSCLE DISEASE

Abstract

Histopathological abnormalities of muscle are common in chronic alcoholics and can be classified into the rare acute myopathy, with myonecrosis, and the much more common chronic myopathy, with a selective atrophy of type II muscle fibres (particularly IIb fibres). The patients may often be asymptomatic and, except for florid cases of acute rhabdomyolysis, clinical features do not help to distinguish the two. Serum creatine kinase activity is an insensitive guide to the presence of the muscle abnormalities. These abnormalities cannot be adequately explained by co-existing alcoholic liver disease, malnutrition or peripheral neuropathy, and probably represent the result of direct toxicity to the muscle fibres. Acute myopathy may occur as a result of damage to cell membranes although intracellular phosphate deficiency has also been proposed as a crucial factor. Atrophy of type II fibres occurs in other metabolic myopathies and its development in chronic alcoholism could represent the result of metabolic or endocrinological derangement induced by ethanol. Alternatively, direct toxicity to muscle cell pathways of carbohydrate catabolism or fatty acid oxidation may occur. Previous suggestions of enhanced muscle breakdown in chronic alcoholics is contested by recent work and reduced protein synthesis may be of more pathogenic importance. Abstention from alcohol reverses the muscle abnormalities.