Division of Endocrinology and Metabolism, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea.
Endocr J. 2010;57(4):347-50. doi: 10.1507/endocrj.k09e-261. Epub 2010 Feb 11.
A 19-year-old girl presented at our emergency room with hypokalemic periodic paralysis. She had a thyrotoxic goiter and had experienced three paralytic attacks during the previous 2 years on occasions when she stopped taking antithyroid drugs. In addition to thyrotoxic periodic paralysis (TPP), she had metabolic acidosis, urinary potassium loss, polyuria and polydipsia. Her reduced ability to acidify urine during spontaneous metabolic acidosis was confirmed by detection of coexisting distal renal tubular acidosis (RTA). The polyuria and polydipsia were caused by nephrogenic diabetes insipidus, which was diagnosed using the water deprivation test and vasopressin administration. Her recurrent and frequent paralytic attacks may have been the combined effects of thyrotoxicosis and RTA. Although the paralytic attack did not recur after improving the thyroid function, mild acidosis and nephrogenic DI have been remained subsequently. Patients with TPP, especially females with atypical metabolic features, should be investigated for possible precipitating factors.
一位 19 岁女孩因低钾周期性麻痹到我院急诊就诊。她患有甲状腺功能亢进性甲状腺肿，在过去 2 年中有 3 次在停止服用抗甲状腺药物时出现麻痹发作。除了甲状腺毒性周期性麻痹（TPP）外，她还伴有代谢性酸中毒、尿钾丢失、多尿和多饮。在自发代谢性酸中毒期间，她的尿液酸化能力降低，这通过同时存在的远端肾小管酸中毒（RTA）得到证实。多尿和多饮是由于肾性尿崩症引起的，通过禁水试验和血管加压素给药诊断了这种疾病。她反复且频繁的麻痹发作可能是甲状腺毒症和 RTA 的共同作用。尽管改善甲状腺功能后麻痹发作未再复发，但随后仍存在轻度酸中毒和肾性尿崩症。TPP 患者，尤其是具有非典型代谢特征的女性，应调查可能的诱发因素。
