To determine the prevalence of alcoholic myopathy and cardiomyopathy, we studied a group of 50 asymptomatic alcoholic men (mean age, 38.5 years) entering an outpatient treatment program. Studies performed included an assessment of muscle strength by electronic myometer, muscle biopsy, echocardiography, and radionuclide cardiac scanning, with comparison to healthy control subjects of similar age. The patients' mean (+/- SEM) daily alcohol consumption was 243 +/- 13 g over an average of 16 years. These patients had no clinical or laboratory signs of malnutrition or electrolyte imbalance. Forty-two percent of the patients, as compared with none of the controls, had strength of less than 20 kg as measured in the deltoid muscle. Muscle-biopsy specimens from 23 patients (46 percent) had histologic evidence of myopathy. In the cardiac studies, when the alcoholic patients were compared with 20 healthy controls, the patients had a significantly lower mean ejection fraction (59 vs. 67 percent), a lower mean shortening fraction (33 vs. 38 percent), a greater mean end-diastolic diameter (51 vs. 49 mm), and a greater mean left ventricular mass (123 vs. 106 g per square meter of body-surface area). One third of the alcoholics had an ejection fraction of 55 percent or less, as compared with none of the controls. Endomyocardial biopsy specimens from six patients with ejection fractions below 50 percent showed histologic changes of cardiomyopathy. The estimated total lifetime dose of ethanol correlated inversely with muscular strength (r = -0.65; P less than 0.001). In an analysis that also included six patients with symptomatic alcoholic cardiomyopathy, the estimated total lifetime dose of ethanol correlated inversely with the ejection fraction (r = -0.58; P less than 0.001) and directly with the left ventricular mass (r = 0.59; P less than 0.001). We conclude that myopathy of skeletal muscle and cardiomyopathy are common among persons with chronic alcoholism and that alcohol is toxic to striated muscle in a dose-dependent manner.

Respiratory and skeletal (deltoid) muscle strength were evaluated in 34 oral steroid-dependent asthmatics by use of maximal inspiratory and expiratory pressures and a myometer. The patients were compared to age- and sex-matched asthmatics who had never been on continuous oral steroid treatment. Endurance time was also studied in ten steroid-dependent asthmatics and ten controls using a pressure threshold breathing device. Nutritional status was assessed from body weight, midarm circumference, triceps skinfold (TSF), prealbumin, albumin, and total protein. An open biopsy from deltoid muscle was taken from nine steroid-dependent asthmatics and the diameter of type 1 and type 2 fibers was measured by a morphometric study. No differences were found between study and control groups either in respiratory and skeletal muscle strength or in endurance time. Steroid-dependent asthmatics showed a decrease in TSF, total protein, albumin, and potassium serum levels when compared with the control group but differences were not statistically significant after Bonferroni's adjustment for multiple comparison studies. Transversal diameter of type 2 fibers was significantly correlated with the percentage of ideal weight (r = 0.75 p less than 0.05), but not with average daily dose of steroids nor with the length of steroid treatment. Our results support the clinical impression that steroids, at the doses usually administered in chronic severe asthma, do not cause muscular weakness. We also found that malnutrition rather than corticosteroids is the most important contributory factor to type 2 muscle fiber atrophy in steroid-dependent asthma.

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Damage of skeletal muscle in association with graft-versus-host disease (GvHD) has been referenced exceptionally. Eighteen months after bone marrow transplantation, a 22-year-old man developed polymyositis associated with manifestations of chronic GvHD, such as peripheral eosinophilia and localized morphea. Diagnosis of polymyositis was established by clinical, electromyographic, and histopathologic findings. His clinical condition improved with immunosuppressive therapy. At electronmicroscopy, some close and broad contacts between lymphocytes with activated appearance and degenerated muscle fibers were observed, suggesting a lymphocytotoxic mechanism. The findings support the idea that polymyositis can be considered a manifestation of chronic GvHD.

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