Abstract
Several clinical trials indicate a dramatic loss of bone mineral density culminating in osteoporosis during long–term therapy with valproate (VPA). There is no agreement on the underlying mechanism, since VPA caused different effects on blood markers of calcium and bone metabolism in several trials. Possible mechanisms are renal tubular dysfunction, interference of electric coupling between osteoblasts, a decrease of IGF–1 production and an imbalance between activation of osteoblasts and osteoclasts. Different recommendations on treatment of VPA–induced osteopenia are summarized. In conclusion, measurement of bone mineral density at regular intervals as well as individual therapy in collaboration with a specialist for bone metabolism is advisable.
Zusammenfassung
Mehrere Studien zeigen unter Langzeittherapie mit Valproat (VPA) eine dramatische Abnahme der Knochendichte bis hin zur Osteoporose. Über den zugrundeliegenden Mechanismus besteht Uneinigkeit, da sich die Auswirkungen von VPA auf biochemische Marker des Kalzium– und Knochenstoffwechsels in den durchgeführten Untersuchungen unterschiedlich darstellten. Diskutiert werden eine renal–tubuläre Dysfunktion, Beeinflussung der elektrischen Kopplung von Osteoblasten, Abnahme der IGF–1–Produktion und eine Erhöhung des Knochenumbaus mit Verschiebung des Aktivierungsgleichgewichts zwischen Osteoblasten und Osteoklasten zugunsten letzterer. Auch für die Therapie der VPA–induzierten Osteopenie gibt es unterschiedliche Empfehlungen. Regelmäßige Knochendichtemessungen und eine individuell abgestimmte Therapie in Zusammenarbeit mit einem Knochenspezialisten ist ratsam.
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Rosenow, F., Hamer, H. & Bauer, S. Valproat und Knochenstoffwechsel. Z. Epileptol. 18, 170–173 (2005). https://doi.org/10.1007/s10309-005-0142-4
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DOI: https://doi.org/10.1007/s10309-005-0142-4