Zusammenfassung
Dem Diabetes liegen Defekte in der Synthese, Sekretion und/oder Wirkung von Insulin zugrunde. Dies kann auf einer Zerstörung der ß-Zellen des Pankreas durch Autoimmunprozesse (Typ 1) oder einer verminderten Insulinempfindlichkeit in Verbindung mit einer gestörten Insulinsekretion der ß-Zelle (Typ 2) beruhen. Ziel der Therapie ist es, durch Substitution des absoluten Insulinmangels und Verbesserung der Insulinwirkung die konsekutiven Störungen im Kohlenhydrat-, Eiweiß-, Fett- und Mineralstoffwechsel so weit als möglich zu normalisieren, um dem Diabetiker als bedingt Gesundem ein normales Leben in Familie, Beruf und Gesellschaft zu ermöglichen. Kurzfristig sollen ketoazidotische Entgleisungen, Infektionen und Hypoglykämien vermieden werden, langfristig gilt es die Spätkomplikationen (Makroangiopathie; Mikroangiopathie: Retinopathie, Nephropathie, diabetischer Fuß; Neuropathie) zu verhindern (primäre Prävention). Es gibt heute umfangreiche Daten aus epidemiologischen Studien, die nachweisen, dass die diabetesspezifischen Spätkomplikationen von der Qualität der Diabeteseinstellung, gemessen an HbA1C und Blutglukose [1, 2], und die Makroangiopathie von der Kontrolle assoziierter Risikofaktoren (wie Hypertonie [3] und Dyslipoproteinämie [4, 5]) abhängen. Davon ausgehend hat die Amerikanische Diabetesgesellschaft Zielgrößen definiert (Tabelle 17.1; [6]), die nach Möglichkeit bis in das Alter angestrebt werden sollen, da auch im hohen Alter die Lebensqualität noch wesentlich von der Diabeteseinstellung abhängt. Wie die Ergebnisse mehrerer Studien [1, 2, 4, 5] zeigen, kann nur durch eine strikte Euglykämisierung und Optimierung der LDL-Cholesterinwerte sowie des Blutdrucks eine Verbesserung der Prognose der Typ-2-Diabetiker erreicht werden.
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Hanefeld, M., Fischer, S. (2000). Therapie des Diabetes mellitus. In: Frölich, J.C., Kirch, W. (eds) Praktische Arzneitherapie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-09398-6_17
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DOI: https://doi.org/10.1007/978-3-662-09398-6_17
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