N Yokota, T Uchida, A Sasaki, K Kobayashi, O Kida, Y Yamamoto, T Eto, K Tanaka
{"title":"甲状腺毒性周期性麻痹合并原发性醛固酮增多症。","authors":"N Yokota, T Uchida, A Sasaki, K Kobayashi, O Kida, Y Yamamoto, T Eto, K Tanaka","doi":"10.2169/internalmedicine1962.30.219","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":14798,"journal":{"name":"Japanese journal of medicine","volume":"30 3","pages":"219-23"},"PeriodicalIF":0.0000,"publicationDate":"1991-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.2169/internalmedicine1962.30.219","citationCount":"8","resultStr":"{\"title\":\"Thyrotoxic periodic paralysis complicated with primary aldosteronism.\",\"authors\":\"N Yokota, T Uchida, A Sasaki, K Kobayashi, O Kida, Y Yamamoto, T Eto, K Tanaka\",\"doi\":\"10.2169/internalmedicine1962.30.219\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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.</p>\",\"PeriodicalId\":14798,\"journal\":{\"name\":\"Japanese journal of medicine\",\"volume\":\"30 3\",\"pages\":\"219-23\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1991-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.2169/internalmedicine1962.30.219\",\"citationCount\":\"8\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Japanese journal of medicine\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2169/internalmedicine1962.30.219\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Japanese journal of medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2169/internalmedicine1962.30.219","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
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.