Shintani S, Shiigai T, Tsukagoshi H
Department of Neurology, Toride Kyodo General Hospital, Ibaraki, Japan.
Eur Neurol. 1991;31(6):396-8. doi: 10.1159/000116702.
A 74-year-old male was admitted to hospital with acute rhabdomyolysis and myoglobinuria due to hypokalemia. The hypokalemia resulted from diuretic treatment. He had no family history of myopathy, and no diarrhea and vomiting. The neurological examination revealed painful quadriplegia. The blood pressure was 160/74 mm Hg. Laboratory examination showed hypokalemic and hypochloremic metabolic alkalosis (serum K 1.5 mEq/l, serum Cl 89 mEq/l, base excess + 20.9, HCO3- 44.9 mmol/l, pH 7.563) and marked elevations of serum CPK, LDH, GOT, GPT and myoglobin. Endocrinological and renal functions were normal. Muscle biopsy revealed marked necrosis with remarkable phagocytosis and vacuolar degeneration. The cessation of diuretics and intravenous infusion of potassium chloride resulted in a marked improvement in clinical and laboratory findings. The diuretics-induced hypokalemic myopathy is rare in the literature.
一名74岁男性因低钾血症导致急性横纹肌溶解和肌红蛋白尿入院。低钾血症是由利尿剂治疗引起的。他没有肌病家族史,也没有腹泻和呕吐。神经系统检查显示四肢疼痛性瘫痪。血压为160/74 mmHg。实验室检查显示低钾低氯性代谢性碱中毒(血清钾1.5 mEq/l,血清氯89 mEq/l,碱剩余+20.9,HCO3- 44.9 mmol/l,pH 7.563),血清CPK、LDH、GOT、GPT和肌红蛋白显著升高。内分泌和肾功能正常。肌肉活检显示明显坏死,伴有显著吞噬作用和空泡变性。停用利尿剂并静脉输注氯化钾后,临床和实验室检查结果显著改善。利尿剂引起的低钾性肌病在文献中较为罕见。