Rassouli M E, Ikeda H, Otsuki S
Folia Psychiatr Neurol Jpn. 1976;30(4):505-15. doi: 10.1111/j.1440-1819.1976.tb02673.x.
A patient with hypokalemic myopathy occurring in the context of chronic alcoholism was reported. A 56-year-old male patient, heavy drinker for 20 years, complained of marked weakness and acutely developing pains in his limbs. The principal clinical findings were weakness and tenderness of the proximal limbs and girdle muscle. He was unable to lift his head or any extremities from the bed. Deep tendon reflexes were diminished, but not absent. There was no sensory disturbance except for muscle tenderness. These clinical manifestations disappeared gradually by abstinence from drinking, and potassium administration therapy, and the patient recovered completely on the 26th day after onset. On the day after admission (8th day), serum potassium value was 2.2 mEq/L, and serum CPK activity was 4270 IU. The ECG pattern was consistent with a diagnosis of low potassium content in serum, and the EMG pattern was consistent with a diagnosis of myopathy. These electrophysiological findings had a tendency to recover from this pattern to normal range correspondingly with clinical improvement. The repeated muscle biopsies showed that vacuolation, hyaline degeneration and significant phagocyte infiltration were observed in the muscle on the 9th day after the onset of muscle weakness, and that these pathological findings disappeared almost completely three weeks later. The frequently repeated examinations of potassium content and CPK activity in sera showed that there was a close correlation between these biochemical abnormalities and clinical improvement. The pathogenesis of alcoholic myopathy and significance of CPK abnormality in chronic alcoholism were discussed.
报告了一名在慢性酒精中毒背景下发生低钾性肌病的患者。一名56岁男性患者,有20年酗酒史,主诉四肢明显无力和急性发作的疼痛。主要临床发现为近端肢体和带肌无力及压痛。他无法将头或任何肢体从床上抬起。深腱反射减弱,但未消失。除肌肉压痛外无感觉障碍。通过戒酒和补钾治疗,这些临床表现逐渐消失,患者在发病后第26天完全康复。入院次日(第8天),血清钾值为2.2 mEq/L,血清肌酸磷酸激酶(CPK)活性为4270 IU。心电图表现符合血清低钾诊断,肌电图表现符合肌病诊断。随着临床改善,这些电生理发现有从该表现恢复到正常范围的趋势。多次肌肉活检显示,肌无力发作后第9天肌肉出现空泡形成、透明变性和大量吞噬细胞浸润,3周后这些病理发现几乎完全消失。血清钾含量和CPK活性的频繁重复检查表明,这些生化异常与临床改善密切相关。讨论了酒精性肌病的发病机制及慢性酒精中毒中CPK异常的意义。