Osteologie 2019; 28(04): 252-258
DOI: 10.1055/a-1002-4038
Originalarbeit
© Georg Thieme Verlag KG Stuttgart · New York

Osteoporose und Frakturrisiko bei Epilepsie und antiepileptischer Therapie

Osteoporosis and fracture risk in epilepsy and antiepileptic drugs
Sandra Baumann
1   Endonet, Endokrinologische Praxis & Labor, CH-4055 Basel, Schweiz
,
Christian Meier
1   Endonet, Endokrinologische Praxis & Labor, CH-4055 Basel, Schweiz
2   Klinik für Endokrinologie, Diabetologie und Metabolismus, Universitätsspital, CH-4031 Basel, Schweiz
› Author Affiliations
Further Information

Publication History

08/02/2019

08/23/2019

Publication Date:
14 November 2019 (online)

Zusammenfassung

In den letzten Jahren zeigte sich, dass Epilepsie und ihre Behandlung einen negativen Einfluss auf die Knochenmineralisation und den Kalzium-Metabolismus haben. Mehrere Studien fanden eine signifikante Reduktion der Knochendichte (BMD) und ein ansteigendes Frakturrisiko bei Patienten, welche mit enzyminduzierenden Antiepileptika (Phenobarbital, Carbamazepin, Phenytoin) behandelt werden. Es wird angenommen, dass CYP-450-induzierende Antiepileptika diejenigen Enzyme hochregulieren, welche für den Vitamin-D-Stoffwechsel verantwortlich sind und dadurch 25-OH Vitamin D vermehrt in inaktive Metabolite abgebaut wird. Dies führt zu einer verminderten Kalziumresorption und konsekutiv zu einem sekundären Hyperparathyreoidismus. Auch für die neueren Antiepileptika (Oxcarbazepin, Gabapentin und Levetiracetam) weisen neuere Daten auf einen Effekt auf den Knochenstoffwechsel hin. Eine prophylaktische Gabe von ausreichend Kalzium und Vitamin D ist für alle Patienten unter antiepileptischer Therapie (AED) empfohlen. Für Patienten mit Langzeit-Einnahme von AEDs sind Knochendichtemessungen als Osteoporose-Basis-Abklärung angezeigt, insbesondere für diejenigen, welche mit enzyminduzierenden AEDs behandelt werden und/oder andere relevante Frakturrisikofaktoren aufweisen. Einige neuere Studien konnten zeigen, dass bei Patienten, die mit AEDs behandelt werden, eine Bisphosphonat-Therapie zusätzlich zu Kalzium und Vitamin D die Knochendichte verbessern und Frakturen verhindern könnte. Deren genereller Einsatz ist jedoch noch nicht empfohlen und für diejenigen Patienten reserviert, welche ein hohes Fraktur-Risiko aufweisen.

Abstract

There is increasing evidence suggesting that epilepsy and its treatment can have adverse effects on bone mineralization. Many studies have shown a significant reduction in bone mineral density (BMD) and an increased fracture risk in patients treated with antiepileptic drugs (AEDs). It is assumed that CYP-450-inducing antiepileptic drugs (phenobarbital, carbamazepine, phenytoin) lower active vitamin D levels leading to reduced calcium absorption with consecutive secondary hyperparathyroidism. Recent studies also have reported bone-specific effects of newer antiepileptic drugs (oxcarbazepine, gabapentin, levetiracetam). Prophylactic administration of adequate amounts of calcium and vitamin D is recommended for all patients treated with AEDs. BMD measurements should be performed in patients with long-term exposure of AEDs (especially enzyme-inducing AEDs) and with other relevant osteoporosis risk factors. Newer data show a beneficial effect on BMD and incidence of new fractures with prophylactic administration of bisphosphonates in addition to calcium and vitamin D. But their general use is not recommended yet and reserved for patients with a high fracture risk.

 
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