Changes in plasma renin activity and plasma aldosterone in the induced paralytic attack of thyrotroxic periodic paralysis.
Changes in plasma renin activity and plasma aldosterone in the induced paralytic attack of thyrotroxic periodic paralysis.
复制标题
甲状腺激素性周期性麻痹诱发麻痹发作时血浆肾素活性和血浆醛固酮的变化。
DOI：
10.1530/acta.0.0820715
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发表时间：
1976
期刊：
影响因子：
--
通讯作者：
I. Miyamori
中科院分区：
文献类型：
--
作者：
R. Takeda;S. Morimoto;K. Uchida;I. Miyamori
本文观察了7例周期性甲状腺功能亢进性麻痹患者输注葡萄糖和胰岛素（GI）后血清电解质、红细胞压积、血浆肾素活性和血浆醛固酮的变化。在7名患者中，有4名患者在GI输注开始后90分钟内诱发了发展为完全四肢瘫痪的发作。另外两名患者仅产生轻微的腿部麻痹，一名患者未诱发发作。在4例完全性四肢瘫痪患者中，GI输注开始后，血清钠和钾浓度、红细胞压积、血浆肾素活性和血浆醛固酮的平均值立即略有下降。麻痹发作的诱导并不伴随着任何显着的变化，血清钠浓度，红细胞压积，血浆肾素活性和血浆醛固酮的发病前或后15分钟，而血清钾浓度进行性下降，并增加血浆醛固酮与红细胞压积和血浆肾素活性的增加在完全四肢瘫痪的阶段达到峰值水平。另一方面，在输液产生轻微或无腿麻痹的3例患者中，血清钠浓度、红细胞压积、血浆肾素活性和血浆醛固酮的变化不显著，血清钾浓度轻微但不显著降低。这些结果表明，醛固酮增多症可能不是诱发麻痹发作的触发因素，而是一种继发于胃肠道输注引起的容量耗竭和钾稳态变化的现象。
Changes in serum electrolytes, haematocrit, plasma renin activity and plasma aldosterone induced by glucose and insulin (GI) infusion were serially investigated in seven patients with periodic thyrotoxic paralysis. An attack which developed into complete quadriplegia was induced within 90 min after the beginning of the GI infusion in four out of seven patients. Only a slight paralysis of the legs was produced in another two patients and induction of an attack did not materialize in one. In four patients with complete quadriplegia, the mean values of serum sodium and potassium concentrations, haematocrit, plasma renin activity and plasma aldosterone slightly decreased immediately after the beginning of the GI infusion. Induction of a paralytic attack was not accompanied by any significant changes in serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone either 15 min before or after the onset of attack, while the serum potassium concentration progressively decreased, and an increase in plasma aldosterone associated with an increase of haematocrit and plasma renin activity reached a peak level at the stage of complete quadriplegia. On the other hand, in the three patients in whom an infusion produced slight or no paralysis of the legs, changes in the serum sodium concentration, haematocrit, plasma renin activity and plasma aldosterone were insignificant and the serum potassium concentration was slightly but insignificantly decreased. These results suggest that hyperaldosteronism may not be a trigger for the induced paralytic attack but a phenomenon secondary to volume depletion and a change in potassium homoeostasis induced by GI infusion.