Zusammenfassung
Osteoporose ist ein wesentliches Merkmal des chronischen Hyperkortisolismus. Glukokortikoide hemmen die Mineralisation und fördern den Nettoausstrom von Kalzium aus dem Skelett durch direkte Wirkungen auf den Osteozyten [1, 2], aber der Einfluß der Glukokortikoide auf die Homöostase von Kalizium gilt als weitere Ursache für die Mineralsalzverarmung des Knochens. Chronischer Hyperkortisolismus steigert die renale Kalziumausscheidung, und Behandlung mit Glukokortikoiden in pharmakologischer Dosis kann eine Abnahme der Kaliziumabsorption aus dem Verdauungstrakt hervorrufen [3], die offenbar dosisabhängig ist: sie wurde bei Therapie mit niedrigen Erhaltungsdosen nicht beobachtet [4, 5]. Beim endogenen Cushing-Syndrom ergaben frühere Messungen und einzelne Untersuchungen der Kalziumbilanz ebenfalls, daß die Kalziumabsorption erniedrigt war [6, 7]; Sjöberg [8] beobachtete aber bei einer Untersuchung an neun Patienten mit endogenem Cushing-Syndrom, daß die Retention von Kalzium aus einer Testmahlzeit normal war.
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Peerenboom, H. et al. (1981). Endokrinologie. In: Miehlke, K. (eds) Verhandlungen der Deutschen Gesellschaft für innere Medizin. Verhandlungen der Deutschen Gesellschaft für innere Medizin, vol 87. J.F. Bergmann-Verlag, Munich. https://doi.org/10.1007/978-3-642-47092-9_11
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