Evers S, Engelien A, Karsch V, Hund M
Department of Neurology, University of Münster, Germany.
J Neurol Neurosurg Psychiatry. 1998 Feb;64(2):249-52. doi: 10.1136/jnnp.64.2.249.
Besides the hereditary hyperkalaemic paralysis, a secondary form exists which often mimicks Guillain-Barre syndrome. A 62 year old patient is reported on who developed severe hyperkalaemic paralysis on the basis of mild renal failure and additive spironolactone intake. Neurophysiological examinations disclosed normal muscle fibre activity but delayed nerve conduction velocities indicating that the mechanism underlying secondary hyperkalaemic paralysis is different from channelopathies. Haemodialysis led to complete recovery. Review of the medical literature showed that spironolactone intake is the most common cause of secondary hyperkalaemic paralysis. Typical symptoms are flaccid tetraplegia sparing the cranial nerves with only mild or lacking sensory impairment. Symptoms promptly resolve after haemodialysis or after glucose and insulin infusion. Only three out of 18 patients reviewed died, because of cardiopulmonary complications. Thus the prognosis of secondary hyperkalaemic paralysis is good.
除遗传性高钾性麻痹外，还存在一种继发性形式，常酷似吉兰-巴雷综合征。本文报道了一名62岁患者，该患者因轻度肾衰竭并额外服用螺内酯而发生严重的高钾性麻痹。神经生理学检查显示肌纤维活动正常，但神经传导速度延迟，表明继发性高钾性麻痹的潜在机制与通道病不同。血液透析使患者完全康复。医学文献回顾表明，服用螺内酯是继发性高钾性麻痹最常见的病因。典型症状为弛缓性四肢瘫，不累及颅神经，仅有轻度感觉障碍或无感觉障碍。血液透析或输注葡萄糖和胰岛素后症状迅速缓解。在回顾的18例患者中，仅3例因心肺并发症死亡。因此，继发性高钾性麻痹的预后良好。
