Proximal myopathy during beta-blockade
Proximal myopathy during beta-blockade
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β-阻断期间的近端肌病
DOI：
10.1136/bmj.280.6211.399-b
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发表时间：
1980
影响因子：
--
通讯作者：
R. Cull
中科院分区：
文献类型：
--
作者：
J. C. Forfar;G. J. Brown;R. Cull
一名68岁的女性于1977年1月开始每8小时服用索他洛尔80 mg。4年的心绞痛病史以前曾用亚硝酸盐治疗。静息心电图正常，运动时出现1-2 mm缺血性ST段压低，心率为130/min。胸片、血浆尿素、电解质和全血细胞计数正常（第1小时ESR 27 mm）。六个月后，她出现手臂和腿部无痛性无力。早上的症状最严重：她不得不爬上楼，不能在没有支撑的情况下站立。在检查中，四头肌组的近端肌无力最明显。臂反射正常，腿反射增强。检查显示全血细胞计数、血浆尿素、电解质、肝功能检查、钙、磷酸盐、血清总甲状腺素和促甲状腺激素释放激素反应正常。类风湿因子和抗核因子均呈阴性。红细胞沉降率（ESR）升高，在第一个小时内从49 mm变化到75 mm。治疗改为普萘洛尔40 mg，每8小时一次，但肌无力持续。普萘洛尔治疗6个月后估计的血清肌酸磷酸激酶（SCPK）浓度升高，范围为700 - 2200 U/l（参考范围30-150 U/l）。同工酶分析表明，其来源主要是骨骼肌。使用同心针电极的肌电图（EMG）显示左胫骨前肌或左三角肌无异常。左侧股四头肌无自发活动：运动单位动作电位以正常幅度（0-5-2 mV）为主，持续时间多为8-10 ms，但短电位（<5 ms）数量增加，其中一些为多相。招聘是充分的，使神经性原因的弱点不太可能。这些变化表明是轻度肌病。广泛的调查，以确定一个隐匿性肿瘤是阴性的。普萘洛尔于1978年7月停用，近端无力迅速消退，SCPK浓度恢复正常（见图）。8月，以每8小时80 mg的剂量重新开始，患者一直保持良好，直到1978年11月，虚弱随着骨骼肌来源的SCPK增加而恢复（见图）。重复肌电图显示左四头肌如上所述的变化，休息时左胫骨前肌也有间歇性纤颤。左侧三角肌外观保持正常。
A 68-year-old woman started taking sotalol 80 mg every eight hours in January 1977. A four-year history of angina of effort had previously been managed with nitrites. The resting electrocardiogram was normal, and with exercise 1-2 mm ischaemic ST depression developed at a heart rate of 130/min. Chest radiograph, plasma urea, electrolytes, and full blood count were normal (ESR 27 mm in the first hour). Six months later she developed painless weakness of the arms and legs. The symptoms were worst in the morning: she had to crawl upstairs and could not stand unsupported. On examination striking proximal muscle weakness was most pronounced in the quadriceps group. Arm reflexes were normal and leg reflexes present with reinforcement. Investigations showed normal full blood count, plasma urea, electrolytes, liver function tests, calcium, phosphate, serum total thyroxine, and thyrotrophin response to thyrotrophin-releasing hormone. Rheumatoid and antinuclear factors were negative. The erythrocyte sedimentation rate (ESR) was raised, varying from 49 to 75 mm in the first hour. Treatment was changed to propranolol 40 mg eight hourly but muscle weakness continued. Serum creatine phosphokinase (SCPK) concentrations, estimated after six months of propranolol treatment, were raised and varied from 700 to 2200 U/l (reference range 30-150 U/1). Isoenzyme estimation showed that its origin was predominantly skeletal muscle. Electromyography (EMG) using a concentric needle electrode showed no abnormalities in the left tibialis anterior or left deltoid. There was no spontaneous activity in the left quadriceps: motor unit action potentials were mainly of normal amplitude (0-5-2 mV) and mostly lasted 8-10 ms. There was, however, an increased number of briefer potentials (< 5ms), some of which were polyphasic. Recruitment was full, making a neuropathic cause for the weakness unlikely. The changes suggested a mild myopathic process. Extensive investigations to identify an occult neoplasm were negative. Propranolol was discontinued in July 1978 and the proximal weakness rapidly resolved and SCPK concentrations returned to normal (see figure). It was reintroduced in August at a dose of 80 mg eight hourly and the patient remained well until November 1978, when weakness returned with an increase in SCPK of skeletal muscle origin (see figure). Repeat EMG showed changes as described above in the left quadriceps and also intermittent fibrillation in the left tibialis anterior at rest. Appearances in the left deltoid remained normal.