Skeletal muscle changes in chronic alcoholic patients. A conventional, histochemical, ultrastructural and morphometric study.
Muscle biopsies of 20 alcoholic patients (15 males and 5 females), most of whom had liver disease and with no clinical or analytical evidence of neuromyopathy, were studied. 10 abstemious patients with no neuromuscular disease were selected as controls. Conventional histology failed to show significant skeletal muscle changes. A characteristic histochemical picture of tubular aggregates was found in one patient. An enlargement of the intermyofibrillar space with increase in glycogen deposition and fat droplets were detected ultrastructurally while 2 of the patients showed tubular aggregates. The mitochondriae of the alcoholic patients had a smaller perimeter and area than those of the control group (P less than 0.004 and P less than 0.008, respectively). These results suggest that the prolonged ingestion of alcohol can cause a mitochondrial alteration only evidenced by morphometry, with poor clinical, biochemical, electrophysiological and histological expression of myopathy. These findings can represent an early stage of alcoholic skeletal muscle injury.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000328:Adult; D000437:Alcoholism / Q000473:pathology*; D001706:Biopsy; D005260:Female; D006003:Glycogen / Q000378:metabolism; D006801:Humans; D050356:Lipid Metabolism; D008104:Liver Cirrhosis, Alcoholic / Q000473:pathology; D008297:Male; D008875:Middle Aged; D008931:Mitochondria, Muscle / Q000648:ultrastructure; D009132:Muscles / Q000473:pathology*; D009210:Myofibrils / Q000648:ultrastructure; D009220:Myositis / Q000473:pathology
D006003:Glycogen; D000251:Adenosine Triphosphatases