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低钾血症和麻痹的罕见病因。

Unusual causes of hypokalaemia and paralysis.

作者信息

Alazami M, Lin S-H, Cheng C-J, Davids M R, Halperin M L

机构信息

University of Toronto, St Michael's Hospital Annex, Lab #1, Research Wing, 38 Shuter Street, Toronto, Ontario M5B 1A6, Canada.

出版信息

QJM. 2006 Mar;99(3):181-92. doi: 10.1093/qjmed/hcl011. Epub 2006 Feb 9.

DOI:10.1093/qjmed/hcl011
PMID:16469765
Abstract

We demonstrate how the application of physiological principles may help to identify unusual causes of a very low plasma potassium (K+) concentration (P(K)) and paralysis. In the two patients described, the short time course of the illness suggested that there was an acute shift of K+ into cells. The combination of a low rate of excretion of K+, the absence of a metabolic acid-base disorder, and the fact that the clinical findings occurred very soon after a large intake of carbohydrate supported this impression. Surprisingly, the P(K) remained low for many hours after these stimuli to shift K+ into cells had abated. The missing link in this story was eventually provided by the attending medical team with the help of their mentor, Professor McCance.

摘要

我们展示了生理学原理的应用如何有助于识别血浆钾(K+)浓度极低(P(K))和瘫痪的异常原因。在所描述的两名患者中,疾病的短病程表明K+急性转移到细胞内。K+排泄率低、不存在代谢性酸碱紊乱以及在大量摄入碳水化合物后很快出现临床症状这一事实支持了这一观点。令人惊讶的是,在这些促使K+转移到细胞内的刺激减弱后,P(K)仍持续低水平数小时。这个故事中缺失的环节最终在他们的导师麦坎斯教授的帮助下由主治医疗团队找到了。

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Unusual causes of hypokalaemia and paralysis.低钾血症和麻痹的罕见病因。
QJM. 2006 Mar;99(3):181-92. doi: 10.1093/qjmed/hcl011. Epub 2006 Feb 9.
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[Etiopathogenetic considerations in 2 cases of dysmetabolic hypokalemic paralysis with signs of increased neuromuscular excitability during potassium repletion].[2例代谢紊乱性低钾性麻痹在补钾过程中出现神经肌肉兴奋性增加体征的病因学思考]
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