Sharma S C, Ray R C, Banerjee A K, Lakshmanan C
Command Pathology Laboratory (CC), Lucknow.
Indian J Pathol Microbiol. 1990 Jul;33(3):244-9.
A comparative histochemical and biochemical study of the anterior tibial muscle of 10 alcoholics suggests that neuropathy could be the cause of chronic muscle weakness and wasting. Myopathic changes did not predominate in the findings. It is concluded that the proximal muscle atrophy could also be attributed to neurogenic damage. Histochemical reactions in muscle specimens show a selective type 2 atrophy and a slight increase in the mean diameter of type 1 fibres. Biochemical investigations reveal that the activities of a number of enzymes representative of energy supplying pathways--the glycogenolysis and glycolysis--as well as acid phosphatase activity in the muscle is lowered. Oxidative enzymes are of similar activity in the alcoholics and the control group. The glycolytic enzyme activity is particularly important, being the most sensitive indicators of the onset, intensity, and course of neurogenic damage.
一项针对10名酗酒者胫骨前肌的组织化学与生物化学对比研究表明，神经病变可能是慢性肌肉无力和萎缩的原因。在研究结果中，肌病性改变并不占主导。得出的结论是，近端肌肉萎缩也可归因于神经源性损伤。肌肉标本的组织化学反应显示出2型纤维选择性萎缩，1型纤维平均直径略有增加。生物化学研究表明，代表能量供应途径的多种酶——糖原分解和糖酵解——以及肌肉中的酸性磷酸酶活性均降低。酗酒者和对照组的氧化酶活性相似。糖酵解酶活性尤为重要，是神经源性损伤的发生、强度和病程的最敏感指标。
