{"title":"[等钾性周期性麻痹]。","authors":"T. Kurihara","doi":"10.32388/q2z84j","DOIUrl":null,"url":null,"abstract":"An autosomal dominant inherited non-dystrophic myotonia caused by mutations of the SCN4A gene, resulting in sodium muscle channelopathy. Currently, it is considered a variant of hyperkalemic periodic paralysis. Patients with normokalemic periodic paralysis do not have any change in their potassium levels during weakness, but become weak when they ingest potassium.","PeriodicalId":79374,"journal":{"name":"Ryoikibetsu shokogun shirizu","volume":"72 1","pages":"134-6"},"PeriodicalIF":0.0000,"publicationDate":"2020-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"[Normokalemic periodic paralysis].\",\"authors\":\"T. Kurihara\",\"doi\":\"10.32388/q2z84j\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"An autosomal dominant inherited non-dystrophic myotonia caused by mutations of the SCN4A gene, resulting in sodium muscle channelopathy. Currently, it is considered a variant of hyperkalemic periodic paralysis. Patients with normokalemic periodic paralysis do not have any change in their potassium levels during weakness, but become weak when they ingest potassium.\",\"PeriodicalId\":79374,\"journal\":{\"name\":\"Ryoikibetsu shokogun shirizu\",\"volume\":\"72 1\",\"pages\":\"134-6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-02-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Ryoikibetsu shokogun shirizu\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.32388/q2z84j\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Ryoikibetsu shokogun shirizu","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.32388/q2z84j","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
An autosomal dominant inherited non-dystrophic myotonia caused by mutations of the SCN4A gene, resulting in sodium muscle channelopathy. Currently, it is considered a variant of hyperkalemic periodic paralysis. Patients with normokalemic periodic paralysis do not have any change in their potassium levels during weakness, but become weak when they ingest potassium.
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