Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis
Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis
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DOI：
10.1046/j.1468-1331.2001.00303.x
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发表时间：
2001-11-01
影响因子：
5.1
通讯作者：
Peters, TJ
中科院分区：
文献类型：
--
作者：
Preedy, VR;Adachi, J;Peters, TJ
酗酒者经常出现步态困难，以及各种肌肉症状，如抽筋、局部疼痛和肌肉质量下降。这些症状在酗酒患者中很常见，以前被认为是源于神经病理的。然而，酒精滥用的直接后果是酒精患者会出现生化损害和/或明确的肌病。肌病的发生与周围神经病变、营养不良和明显的肝病无关。慢性酒精性肌病的特征是II型纤维的选择性萎缩，整个肌肉质量可能减少30%。这种肌病可以说是西半球最常见的骨骼肌疾病，大约50%的酗酒者会发生这种疾病。酒精和乙醛是肌肉蛋白质合成的有效抑制剂，无论是收缩蛋白还是非收缩蛋白都受到急性和慢性酒精剂量的影响。肌肉RNA也通过增加核糖核酸酶活性的机制减少。一般说来，尽管肌膜损伤的标志物增加了，但肌肉蛋白水解酶活性降低或没有改变，这可能与活性氧的损伤有关。这一假设得到了以下观察的支持，即在英国，肌病酗酒者的α-生育酚状态很差。减少的α-生育酚可能会使肌肉预先受到代谢性损伤。然而，试验性的α-生育酚补充在预防酒精诱导的肌肉损伤方面无效，其定义是蛋白质合成速度降低，在患有肌病的西班牙酒精患者中，没有证据表明α-生育酚状态受损。总而言之，酒精通过一系列复杂的机制对骨骼肌产生不利影响。除了肌肉的机械变化，还有重要的代谢后果，这是因为骨骼肌占体重的40%，是整个身体蛋白质周转的重要贡献者。
Alcohol misusers frequently have difficulties in gait, and various Muscle Symptoms such as cramps, local pain and reduced muscle mass. These symptoms are common in alcoholic patients and have previously been ascribed as neuropathological in origin. However, biochemical lesions and/or the presence of a defined myopathy occur in alcoholics as a direct consequence of alcohol misuse. The myopathy occurs independently of peripheral neuropathy, malnutrition and overt liver disease. Chronic alcoholic myopathy is characterized by selective atrophy of Type II fibres and the entire muscle mass may be reduced by up to 30%. This myopathy is arguably the most prevalent skeletal muscle disorder in the Western Hemisphere and occurs in approximately 50% of alcohol misusers. Alcohol and acetaldehyde are potent inhibitors of muscle protein synthesis, and both contractile and non-contractile proteins are affected by acute and chronic alcohol dosage. Muscle RNA is also reduced by mechanisms involving increased RNase activities. In general, muscle protease activities are either reduced or unaltered, although markers of muscle membrane damage are increased which may be related to injury by reactive oxygen species. This supposition is supported by the observation that in the UK, alpha -tocopherol status is poor in myopathic alcoholics. Reduced alpha -tocopherol may pre-dispose the muscle to metabolic injury. However, experimental alpha -tocopherol supplementation is ineffective in preventing ethanol-induced lesions in muscle as defined by reduced rates of protein synthesis and in Spanish alcoholics with myopathy, there is no evidence of impaired alpha -tocopherol status. In conclusion, by a complex series of mechanisms, alcohol adversely affects skeletal muscle. In addition to the mechanical changes to muscle, there are important metabolic consequences, by virtue of the fact that skeletal muscle is 40% of body mass and an important contributor to whole-body protein turnover.