Prophylaxe und Therapie der Glukokortikoid-induzierten Osteoporose

Zusammenfassung

Die Glukokortikoid-induzierte Osteoporose (GK-OP) ist eine der häufigsten Formen der Osteoporose. Epidemiologischen Untersuchungen zufolge nehmen 0,5–0,9% der Bevölkerung Glukokortikoide (GK) ein, bei den über 50-jährigen liegt diese Zahl bei ca. 3%. Das Frakturrisiko ist unter chronischer GK-Therapie auf das Doppelte erhöht und liegt auf Grund der bevorzugten Wirkung von GK auf den trabekulären Knochen für Wirbelkörperfrakturen noch höher. Pathogenetisch liegt der GK-OP eine Verminderung von Knochenmasse und – qualität zugrunde, welche aus suppressiven Effekten von GK auf die Zahl und Funktion von Osteoblasten und Osteocyten und einer Steigerung der Knochenresorption resultiert. Systemische Effekte welche zu Sarkopenie mit erhöhtem Sturzrisiko, hormonellen Veränderungen und negativer Kalziumbilanz führen, können die ungünstigen Wirkungen von GK auf den Knochen weiter amplifizieren. Eine Osteoporose-Basisdiagnostik inklusive Osteodensitometrie sollte immer dann erfolgen, wenn mit einer GK-Therapie von mindestens 2,5 mg/d Prednisolonäquivalent über mehr als 3 Monate zu rechnen ist. Das Frakturrisiko ist bereits nach 3 Monaten GK-Therapie erhöht. Daher ist eine frühzeitige Intervention zur Hemmung des GK-induzierten Knochenmasseverlustes angezeigt. Die Leitlinien des Dachverbandes osteologischer Gesellschaften (DVO) liefern die Grundlage für eine am kalkulierten Frakturrisiko orientierte Prophylaxe und Therapie der GK-OP. Zu den allgemeinen Maßnahmen zählen Sturzprävention und Verbesserung von Muskelmasse und Koordination ebenso wie eine ausreichende Versorgung mit Kalzium und Vitamin D. Die Indikationsstellung für eine über diese Maßnahmen hinausgehende spezifische medikamentöse Therapie basiert auf dem individuellen Frakturrisiko, welches entscheidend durch GK-Dosis und Dauer der Therapie, Alter, Geschlecht und weitere Risikofaktoren einschließlich der mit GK behandelten Grunderkrankung bestimmt wird. Für die Umsetzung der Empfehlungen ist insbesondere im prophylaktischen Ansatz eine Kalkulation der geplanten GK-Dauer und Dosis essentiell. In diesem Zusammenhang bieten die Leitlinien zur Therapie der verschiedenen entzündlich rheumatischen Erkrankungen eine wichtige Orientierungshilfe. Bei GK-Dosen von≥7,5 PubMed mg/d Prednisolonäquivalent über mehr als 3 Monate ist eine spezifische medikamentöse Therapie bei einem T-Score von<− 1,5 bzw. beim Vorliegen einer niedrig-traumatischen Wirbelkörperfraktur oder multipler peripherer Frakturen indiziert. GK-Dosen zwischen 2,5 und 7,5 mg/d bedingen eine Absenkung der durch Alter, Geschlecht und weitere Risikofaktoren bestimmten Therapieschwelle. Eine Prävention des GK-induzierten Knochenmasseverlustes und von vertebralen Frakturen wurde sowohl für Bisphosphonate als auch für Teriparatid nachgewiesen.Bisphosphonate eignen sich insbesondere zur Prävention, Teriparatid zur Behandlung der schweren Osteoporose mit prävalenten Frakturen. Entscheidend ist eine noch konsequentere Umsetzung der Empfehlungen zur Prophylaxe und Therapie der GK-OP.

Abstract

Glucocorticoid-induced osteoporosis (GC-OP) is one of the most frequent forms of osteoporosis. Based on epidemiological investigations, 0.5–0.9% of the community population use oral glucocorticoids (GC); in persons aged 50 or more, the number of GC users is about 3%. The fracture risk is increased twofold in patients with chronic GC treatment and is even higher for vertebral fractures because GCs predominantly affect trabecular bone. The pathogenetic origin of GC-OP is a loss of bone mass and quality resulting from the suppressive effects of GC on the number and function of osteoblasts and osteocytes and an increase in bone resorption. Systemic effects inducing sarcopenia with an increased risk of falls, hormonal changes and a negative calcium balance may further amplify the unfavourable effects of GCs on bone. Basic diagnostic evaluation for osteoporosis including osteodensitometry is indicated when GC treatment with a minimum daily dose of 2.5 mg/d prednisolone equivalent is planned for more than 3 months. The fracture risk is already increased in the first 3 months of GC treatment. Therefore an early intervention to prevent GC-induced loss of bone mass is necessary. The guidelines given by the umbrella organisation of the German osteology societies provide the foundation for prophylaxis and treatment of GC-OP based on the calculated fracture risk. General measures include the prevention of falls and improvement of muscle mass and coordination as well as a sufficient supply of calcium and vitamin D. The indication for specific drug treatment exceeding these basic measures depends on the individual fracture risk, which is determined by daily GC dose, duration of GC treatment, age, gender and other risk factors including the underlying disease that is treated with GC. For the implementation of the recommendations, particularly in the prophylactic approach, the calculation of the duration and dose of planned GC treatment is essential. In this context the guidelines for treatment of the different inflammatory rheumatic diseases provide crucial orientation. Treatment with GC doses of≥7.5 mg/d prednisolone equivalent for more than 3 months requires specific drug treatment if T scores are <− 1.5 or if low-traumatic vertebral fractures or multiple peripheral fractures are present. GC doses between 2.5 und 7.5 mg/d require a lowering of the treatment threshold, which is determined by age, gender and other risk factors. A prevention of GC-induced loss of bone mass and vertebral fractures has been shown for bisphosphonates and teriparatide. Bisphosphonates are particularly suitable for prevention, while teriparatide is useful for the treatment of severe osteoporosis with prevalent fractures. A more consistent implementation of the recommendations for prophylaxis and treatment of GC-OP is crucial.

Schlüsselwörter

Glukokortikoid-induzierte Osteoporose - Pathophysiologie - Prophylaxe - medikamentöse Therapie

Key words

Glucocorticoid-induced osteoporosis - pathophysiology - prophylaxis - drug therapy

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