{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2022,4,1]],"date-time":"2022-04-01T19:49:59Z","timestamp":1648842599995},"reference-count":7,"publisher":"Hogrefe Publishing Group","issue":"16","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Praxis"],"published-print":{"date-parts":[[2017,8]]},"abstract":"<jats:p> Zusammenfassung. Beim Morbus Addison handelt es sich um eine prim\u00e4re Nebennierenrindeninsuffizienz mit Glukokortikoid- und Mineralokortikoidmangel. Die h\u00e4ufigste Ursache der prim\u00e4ren Nebennierenrindeninsuffizienz (NNRI) in westlichen L\u00e4ndern ist die Autoimmunadrenalitis (80 %). Weitere Ursachen sind Karzinommetastasen, besonders von Bronchialkarzinomen, malignen Melanomen und Nierenzellkarzinomen. In Entwicklungsl\u00e4ndern gilt die Nierentuberkulose noch immer als die h\u00e4ufigste Ursache der prim\u00e4ren NNRI. Die Klinik besteht aus unspezifischen Allgemeinsymptomen wie M\u00fcdigkeit, Myalgien, \u00dcbelkeit und Gewichtsverlust. Bei fehlender ad\u00e4quater Substitution der Nebennierenhormone besteht die Gefahr einer Addison-Krise. Ausl\u00f6ser der Addison-Krise sind \u00abStresssituationen\u00bb mit erh\u00f6htem Cortisol-Bedarf (z.B. Infekte oder starke k\u00f6rperliche Belastungen). Die Therapie der Addison-Krise besteht in der Gabe von hochdosiertem Hydrocortison. Als Dauertherapie werden Hydrocortison und Fludrocortison verabreicht. <\/jats:p>","DOI":"10.1024\/1661-8157\/a002751","type":"journal-article","created":{"date-parts":[[2017,8,10]],"date-time":"2017-08-10T09:34:20Z","timestamp":1502357660000},"page":"861-868","source":"Crossref","is-referenced-by-count":0,"title":["CME: Morbus Addison"],"prefix":"10.1024","volume":"106","author":[{"given":"T\u00fclay","family":"Yalcin","sequence":"first","affiliation":[{"name":"Klinik f\u00fcr Innere Medizin, Kantonsspital Schaffhausen"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Markus","family":"Schneemann","sequence":"additional","affiliation":[{"name":"Klinik f\u00fcr Innere Medizin, Kantonsspital Schaffhausen"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Beat","family":"Schmid","sequence":"additional","affiliation":[{"name":"Endokrinologie, Klinik f\u00fcr Innere Medizin, Kantonsspital Schaffhausen"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"101","reference":[{"key":"c1","doi-asserted-by":"publisher","DOI":"10.1210\/jc.2015-1710"},{"key":"c2","doi-asserted-by":"publisher","DOI":"10.1016\/S2213-8587(14)70142-1"},{"key":"c3","unstructured":"Stewart P  : The adrenal cortex: Glucocorticoid deficiency. In: Kronenberg HM, Melmed S, Polonsky K, Larsen PR (eds) : Williams textbook of endocrinology ( ed. 11 ). Philadelphia, PA; Saunders\/Elsevier: 477\u2013495."},{"key":"c4","author":"Nieman LK","journal-title":"UpToDate"},{"key":"c5","author":"Nieman LK","journal-title":"UpToDate"},{"key":"c6","author":"Nieman LK","journal-title":"UpToDate"},{"key":"c7","doi-asserted-by":"publisher","DOI":"10.4414\/smf.2016.02798"}],"container-title":["Praxis"],"original-title":[],"language":"de","link":[{"URL":"https:\/\/econtent.hogrefe.com\/doi\/pdf\/10.1024\/1661-8157\/a002751","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2021,3,17]],"date-time":"2021-03-17T08:35:01Z","timestamp":1615970101000},"score":1,"resource":{"primary":{"URL":"https:\/\/econtent.hogrefe.com\/doi\/10.1024\/1661-8157\/a002751"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2017,8]]},"references-count":7,"journal-issue":{"issue":"16","published-print":{"date-parts":[[2017,8]]}},"alternative-id":["10.1024\/1661-8157\/a002751"],"URL":"https:\/\/doi.org\/10.1024\/1661-8157\/a002751","relation":{},"ISSN":["1661-8157","1661-8165"],"issn-type":[{"value":"1661-8157","type":"print"},{"value":"1661-8165","type":"electronic"}],"subject":[],"published":{"date-parts":[[2017,8]]}}}