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Despite the fact that the mean lifetime dose of alcohol in female alcoholics was only 60% that in male alcoholics, cardiomyopathy and myopathy were as common in female alcoholics as in male alcoholics. This finding, together with a more pronounced response of the ejection fraction to the dose of ethanol, indicates that women are more sensitive than men to the toxic effects of alcohol on striated muscle.

High alcohol intake is the main risk factor for developing community-acquired pneumonia in middle-aged people. This situation also confers a worse prognosis in these patients, who should be treated with broad-spectrum antibiotics for a longer period.

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To determine the influence of chronic ethanol intake and nutritional status on cerebellar shrinkage in alcoholism, we studied 12 undernourished patients with acute Wernicke's encephalopathy (WE), 12 undernourished and 24 well-nourished asymptomatic chronic alcoholics, and 24 age-matched well-nourished controls, using morphometric analysis of MRI scans with volumetry of the cerebellum. Alcoholics reported a mean daily intake of ethanol of 177+/-8 g over a period of 27+/-1 years. Most undernourished alcoholics and half of the well-nourished alcoholics, compared to one-tenth of the controls, showed a significant reduction in cerebellar volume (p< or =0.01, both). Alcoholics with cerebellar shrinkage (n=33) were older (p=0.05) and tended to report greater daily ethanol intake than alcoholics without cerebellar shrinkage (n=15), although not significantly so (p=0.09). Cerebellar volume correlated negatively with age in controls and asymptomatic alcoholics (r> or =0.52, p< or =0.01, both), with a significantly greater shrinkage for age in the latter (p=0.003). Logistic regression analysis showed that malnutrition (OR 6.6 [95%CI 1.7-25.6], p=0.005) and a daily ethanol intake of more than 140 g over ten years (OR 6.1 [95%CI 1.8-20.5], p=0.003) were independently associated with the development of cerebellar shrinkage.

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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