{"title":"黏液水肿。","authors":"G. Fitzhugh, L. Cecil","doi":"10.32388/mnkznb","DOIUrl":null,"url":null,"abstract":"This review will discuss generalized myxedema as it develops in hypothyroidism. First, the precipitating conditions (thyroprivic trophoprivic + goitrous forms) and the clinical manifestations of thyroid hormone deficiency are presented. Pathobiochemical and pathophysiological factors that lead to the main manifestations include retention of fluid, retention of sodium and hyponatremia. In particular are primary and direct consequences of reduced thyroid hormone levels, and secondary or indirect consequences, such as cardiovascular and renal derangements. In hypothyroidism many biochemical disturbances result. Most important is the interstitial deposition of hydrophilic mucopolysaccharides, which in turn lead to fluid and Na retention and impairment of blood circulation and lymphatic drainage. Myxedema, therefore, is to a large extent a lymphatic edema. Hyponatremia is an indirect consequence of the lack of T3 and is directly caused by impaired renal Na reabsorption. Renal Na,K-ATPase is reduced in specific segments. The often discussed role of inappropriate elevation of circulating ADH does not seem to be a key factor in myxedema. Impaired capacity of renal water excretion is caused by reduced GFR. We discuss the time dependent development of the derangement of different organ systems, and include recently published biochemical results, according to which the lack of T3 interferes not only with the metabolism of numerous compounds of the interstitial matrix, but also with cell surface proteins and intracellular proteins of microfilaments. Finally, we refer briefly to pretibial myxedema in states of hyperthyroidism, that is, infiltrative dermopathy in Graves' disease, which is caused by poorly understood autoimmune processes.","PeriodicalId":7734,"journal":{"name":"American practitioner and digest of treatment","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Myxedema.\",\"authors\":\"G. Fitzhugh, L. Cecil\",\"doi\":\"10.32388/mnkznb\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"This review will discuss generalized myxedema as it develops in hypothyroidism. First, the precipitating conditions (thyroprivic trophoprivic + goitrous forms) and the clinical manifestations of thyroid hormone deficiency are presented. Pathobiochemical and pathophysiological factors that lead to the main manifestations include retention of fluid, retention of sodium and hyponatremia. In particular are primary and direct consequences of reduced thyroid hormone levels, and secondary or indirect consequences, such as cardiovascular and renal derangements. In hypothyroidism many biochemical disturbances result. Most important is the interstitial deposition of hydrophilic mucopolysaccharides, which in turn lead to fluid and Na retention and impairment of blood circulation and lymphatic drainage. Myxedema, therefore, is to a large extent a lymphatic edema. Hyponatremia is an indirect consequence of the lack of T3 and is directly caused by impaired renal Na reabsorption. Renal Na,K-ATPase is reduced in specific segments. The often discussed role of inappropriate elevation of circulating ADH does not seem to be a key factor in myxedema. Impaired capacity of renal water excretion is caused by reduced GFR. 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Finally, we refer briefly to pretibial myxedema in states of hyperthyroidism, that is, infiltrative dermopathy in Graves' disease, which is caused by poorly understood autoimmune processes.\",\"PeriodicalId\":7734,\"journal\":{\"name\":\"American practitioner and digest of treatment\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2020-02-07\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American practitioner and digest of treatment\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.32388/mnkznb\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American practitioner and digest of treatment","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.32388/mnkznb","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
这篇综述将讨论在甲状腺功能减退症中发生的全面性黏液性水肿。首先介绍了甲状腺激素缺乏症的发病条件(甲状腺营养不良+甲状腺肿形式)和临床表现。导致其主要表现为液体潴留、钠潴留和低钠血症的病理生化和病理生理因素。特别是甲状腺激素水平降低的主要和直接后果,以及继发性或间接后果,如心血管和肾脏紊乱。甲状腺功能减退导致许多生化紊乱。最重要的是亲水性粘多糖的间质沉积,这反过来导致液体和钠潴留,损害血液循环和淋巴引流。因此,黏液性水肿在很大程度上是淋巴水肿。低钠血症是T3缺乏的间接后果,是由肾钠重吸收受损直接引起的。肾Na, k - atp酶在特定节段减少。经常讨论的循环ADH不适当升高的作用似乎不是黏液性水肿的关键因素。肾水排泄能力受损是由GFR降低引起的。我们讨论了不同器官系统紊乱的时间依赖性发展,并包括最近发表的生化结果,根据这些结果,T3的缺乏不仅会干扰间质基质中许多化合物的代谢,还会干扰细胞表面蛋白和微丝细胞内蛋白。最后,我们简要地提到甲状腺功能亢进状态下的胫前黏液水肿,即Graves病的浸润性皮肤病,这是由自身免疫过程引起的。
This review will discuss generalized myxedema as it develops in hypothyroidism. First, the precipitating conditions (thyroprivic trophoprivic + goitrous forms) and the clinical manifestations of thyroid hormone deficiency are presented. Pathobiochemical and pathophysiological factors that lead to the main manifestations include retention of fluid, retention of sodium and hyponatremia. In particular are primary and direct consequences of reduced thyroid hormone levels, and secondary or indirect consequences, such as cardiovascular and renal derangements. In hypothyroidism many biochemical disturbances result. Most important is the interstitial deposition of hydrophilic mucopolysaccharides, which in turn lead to fluid and Na retention and impairment of blood circulation and lymphatic drainage. Myxedema, therefore, is to a large extent a lymphatic edema. Hyponatremia is an indirect consequence of the lack of T3 and is directly caused by impaired renal Na reabsorption. Renal Na,K-ATPase is reduced in specific segments. The often discussed role of inappropriate elevation of circulating ADH does not seem to be a key factor in myxedema. Impaired capacity of renal water excretion is caused by reduced GFR. We discuss the time dependent development of the derangement of different organ systems, and include recently published biochemical results, according to which the lack of T3 interferes not only with the metabolism of numerous compounds of the interstitial matrix, but also with cell surface proteins and intracellular proteins of microfilaments. Finally, we refer briefly to pretibial myxedema in states of hyperthyroidism, that is, infiltrative dermopathy in Graves' disease, which is caused by poorly understood autoimmune processes.