McLoughlin D M, Spargo E, Wassif W S, Newham D J, Peters T J, Lantos P L, Russell G F
Department of Psychiatry, Institute of Psychiatry, London, UK.
Acta Neuropathol. 1998 Jun;95(6):632-40. doi: 10.1007/s004010050850.
Protein-energy malnutrition in anorexia nervosa is an under-recognised cause of muscle dysfunction. To characterise the skeletal myopathy that occurs in patients with severe anorexia nervosa, muscle function and structure were comprehensively examined in eight young adult female patients with severe (40%) self-induced weight loss. All of the patients showed impaired muscle function on strength and exercise measurement. The maximum voluntary contraction force for the patient group was significantly less than predicted values. Electromyography revealed myopathy in five of the patients, four of whom also had electro-physiological evidence of neuropathy. However, muscle biopsy specimens consistently showed myopathic changes with severe type 2 fibre atrophy but with no evidence of neuropathic changes. Ultrastructurally, there was separation and segmental loss of myofibrils and most biopsy samples contained abundant glycogen granules; we have previously reported that one of the most consistent biochemical abnormalities in these patients is impaired ischaemic lactate responses to forearm exercise. The result of severe protein-energy malnutrition on the musculo-skeletal system is a metabolic myopathy. Although the patients admitted to a variety of abnormal dieting behaviours, such as over-exercising and self-induced vomiting, no association was found between any of these and quantitative histological changes in the muscle biopsy samples. It is recommended that myopathy in anorexia nervosa be treated by instituting an appropriate refeeding programme.
神经性厌食症中的蛋白质 - 能量营养不良是肌肉功能障碍的一个未被充分认识的原因。为了描述重度神经性厌食症患者所发生的骨骼肌病，对8名严重（自我导致体重减轻40%）的年轻成年女性患者的肌肉功能和结构进行了全面检查。所有患者在力量和运动测量方面均显示肌肉功能受损。患者组的最大自主收缩力明显低于预测值。肌电图显示5名患者存在肌病，其中4名患者还有神经病变的电生理证据。然而，肌肉活检标本始终显示出肌病性改变，伴有严重的2型纤维萎缩，但没有神经病变的证据。在超微结构上，存在肌原纤维的分离和节段性丢失，并且大多数活检样本含有丰富的糖原颗粒；我们之前报道过，这些患者最一致的生化异常之一是前臂运动时缺血性乳酸反应受损。严重蛋白质 - 能量营养不良对肌肉骨骼系统的影响是一种代谢性肌病。尽管患者承认有各种异常节食行为，如过度运动和自我催吐，但在这些行为与肌肉活检样本的定量组织学变化之间未发现关联。建议通过制定适当的重新喂养计划来治疗神经性厌食症中的肌病。
