Some authors have suggested a possible loss of antioxidant factors in alcoholic skeletal myopathy. To assess the relationship between ethanol consumption and serum and muscle levels of alpha-tocopherol, ascorbic acid, and retinol in chronic alcoholics with and without skeletal myopathy, a prospective cross-sectional study was performed in the Alcohol Unit of a 1000-bed university hospital. Twenty-five chronic male alcoholic patients (10 with skeletal myopathy) and 15 male controls of similar age were included. Evaluation of daily and lifetime ethanol consumption, assessment of anthropometric and protein nutritional parameters, and open biopsy of the left deltoid muscle were performed, as well as determinations of serum and muscle levels of retinol, alpha-tocopherol, and ascorbic acid by HPLC analysis. Ten of the 25 chronic alcoholic patients presented histological criteria of skeletal myopathy. Four alcoholics presented caloric malnutrition and three protein malnutrition. All of the muscle biopsies of the control group were entirely normal, as were their nutritional studies. The serum and muscular levels of alpha-tocopherol, ascorbic acid, and retinol were normal and were similar in both alcoholics and controls. Except for serum retinol, these values were also similar in alcoholic patients with or without skeletal myopathy. In the univariate analysis, we identified the total lifetime dose of ethanol (p < 0.003), the muscle arm area (p < 0.05), and serum levels of prealbumin (p < 0.03) and retinol-binding protein (p < 0.05) as factors influencing the development of alcoholic myopathy. However, in multivariate analysis, the total lifetime dose of ethanol was the only independent factor in relation to alcoholic myopathy (p < 0.003). Serum and muscle levels of the antioxidants alpha-tocopherol, ascorbic acid, and retinol do not influence the presence of skeletal myopathy in chronic alcoholic patients.

Primary lymphomas of the central nervous system (PLCNS) of T-cell lineage are unusual. It has been suggested that T-cell PLCNS, compared to those of B-cell origin, present some differences in relation to age of presentation, gender, location of the tumor and survival. We describe two cases with T-cell PLCNS and review 22 parenchymatous T-cell PLCNS reported in the English literature. Age, gender and survival of the whole series of 24 T-cell PLCNS did not differ from that reported in large series of PLCNS where the great majority were of B-cell origin. In contrast, a location in the posterior fossa was found in 54% of T-cell PLCNS, whereas this location ranged from 12 go 29% in series of, mostly B-cell, PLCNS. T-cell PLCNS had a higher frequency (33%) of the histologic low grade small lymphocytic lymphoma than B-cell PLCNS (5%). Analysis of six T-cell PLCNS long-term survivors showed that half of them had low grade lymphomas. We conclude that T-cell PLCNS do not differ from those of B-cell origin in age of presentation or gender, but they have a preference to develop in the posterior fossa and a higher frequency of low grade histology which would probably explain the longer survival in some patients.

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et al. 1990; Dodd et al. 1992; Freund & Anderson 1996, 1999 Ridge et al. 2008).Our hypothesis is that permanent neuronal damage produced by chronic alcohol consumption is in part due to progressive changes in NMDA receptors, and that these changes might develop before the beginning of clinical manifestations of chronic alcoholism, including dependence, craving and abstinence. Thus, we assessed here the density of NMDA receptors in frontal cortex and hippocampus -brain areas known to be notably affected by chronic alcohol consumption-in a group of 16 alcohol consumers (AC) (16 male, mean age 58±12 years, post-mortem delay 19±8 hours) in comparison to a control group of 16 non-drinkers (14 male and 2 female, mean age 60±12 years, postmortem delay 17±5 hours) using autoradiographic techniques with the specific NMDA-antagonist [ 3 H]MK801. AC subjects included had not suffered any hepatic, neurologic or psychiatric disorders related to alcoholism. They were classified as moderate consumers (40 to 80 g of absolute alcohol daily for at least 10 years) or heavy consumers (more than 80 g of absolute alcohol daily for at least 10 years, enough to develop chronic alcoholic pathology). We also discriminated between AC cases that were abstinent (alcohol withdrawal minimum one week before death) or non-abstinent (last ethanol ingestion less than 12 hours before death). In consequence, it is unlikely that these subjects would undergo a withdrawal situation that could eventually involve acute changes in NMDA receptors (See Supplementary Material for additional information).