甲状腺毒性周期性麻痹合并原发性醛固酮增多症。

N Yokota, T Uchida, A Sasaki, K Kobayashi, O Kida, Y Yamamoto, T Eto, K Tanaka
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引用次数: 8

摘要

一位35岁的男性在摄入大量碳水化合物后出现双侧下肢无力的急性发作。实验室检查显示严重低钾血症(1.9 mEq/l)和甲状腺功能亢进。患者还表现出原发性醛固酮增多症,原因是左肾上腺腺瘤。作为诊断工具,通过葡萄糖输注诱导低钾血症(2.8 mEq/l)瘫痪。在甲巯咪唑治疗后,没有进一步的瘫痪发作,随后用葡萄糖诱导瘫痪是不可能的,尽管原发性醛固酮增多症持续存在。这些发现表明,甲状腺功能亢进在周期性麻痹的发展中起主要作用,而原发性醛固酮增多症显然增加了患者对麻痹发作的脆弱性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Thyrotoxic periodic paralysis complicated with primary aldosteronism.

A 35-year-old man presented with acute onset of bilateral lower extremity weakness after ingesting a large amount of carbohydrates. Laboratory investigation revealed severe hypokalemia (1.9 mEq/l) and hyperthyroidism. The patient also exhibited primary aldosteronism due to a left adrenal adenoma. As a diagnostic tool, paralysis with hypokalemia (2.8 mEq/l) was induced with a glucose infusion. After treatment with methimazole, there were no further episodes of paralysis and subsequent induction of paralysis with glucose was impossible, though primary aldosteronism persisted. These findings indicate that hyperthyroidism played a major role in the development of periodic paralysis, while primary aldosteronism apparently increased the patient's vulnerability to paralytic attacks.

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