Martin F, Peters T J
Alcohol Alcohol. 1985;20(2):125-36.
Histopathological abnormalities of muscle are common in chronic alcoholics and can be classified into the rare acute myopathy, with myonecrosis, and the much more common chronic myopathy, with a selective atrophy of type II muscle fibres (particularly IIb fibres). The patients may often be asymptomatic and, except for florid cases of acute rhabdomyolysis, clinical features do not help to distinguish the two. Serum creatine kinase activity is an insensitive guide to the presence of the muscle abnormalities. These abnormalities cannot be adequately explained by co-existing alcoholic liver disease, malnutrition or peripheral neuropathy, and probably represent the result of direct toxicity to the muscle fibres. Acute myopathy may occur as a result of damage to cell membranes although intracellular phosphate deficiency has also been proposed as a crucial factor. Atrophy of type II fibres occurs in other metabolic myopathies and its development in chronic alcoholism could represent the result of metabolic or endocrinological derangement induced by ethanol. Alternatively, direct toxicity to muscle cell pathways of carbohydrate catabolism or fatty acid oxidation may occur. Previous suggestions of enhanced muscle breakdown in chronic alcoholics is contested by recent work and reduced protein synthesis may be of more pathogenic importance. Abstention from alcohol reverses the muscle abnormalities.
肌肉的组织病理学异常在慢性酒精中毒患者中很常见，可分为罕见的急性肌病（伴有肌坏死）和更为常见的慢性肌病（伴有II型肌纤维，特别是IIb型纤维的选择性萎缩）。患者通常可能没有症状，除了明显的急性横纹肌溶解病例外，临床特征无助于区分这两种情况。血清肌酸激酶活性对肌肉异常的存在是一个不敏感的指标。这些异常不能通过并存的酒精性肝病、营养不良或周围神经病变得到充分解释，可能代表对肌纤维的直接毒性作用。急性肌病可能是细胞膜受损的结果，尽管细胞内磷酸盐缺乏也被认为是一个关键因素。II型纤维萎缩也发生在其他代谢性肌病中，在慢性酒精中毒中其发展可能是乙醇诱导的代谢或内分泌紊乱的结果。或者，可能对肌肉细胞碳水化合物分解代谢或脂肪酸氧化途径产生直接毒性作用。先前关于慢性酒精中毒患者肌肉分解增强的观点受到近期研究的质疑，蛋白质合成减少可能在致病方面更为重要。戒酒可逆转肌肉异常。
