An explorative literature review of the multifactorial causes of osteoporosis in epilepsy

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Purpose: Patients with epilepsy have a greatly increased risk of osteoporosis and fractures. The literature is diverse and contradictory when dealing with the underlying pathophysiological mechanisms. Consequently, the purpose of this review was to shed light on the multifactorial causes behind the increased occurrence of metabolic bone disease in patients with epilepsy and to identify areas for future research. Methods: A review of the literature was performed searching PubMed with relevant Medical Subject Headings MeSH terms. The results of the search were evaluated for relevance to the review based on the title and abstract of the publication. Publications in language other than English and publications pertaining only pediatric patients were excluded. For all studies, included reference lists were evaluated for further relevant publications. In total, 96 publications were included in this explorative review. Results: The high occurrence of metabolic bone disease in patients with epilepsy is multifactorial. The causes are the socioeconomic consequences of having a chronic neurological disease but also adverse effects to antiepileptic drug treatment ranging from interference with calcium and vitamin D metabolism to hyponatremia-induced osteoporosis. Conclusion: The literature supports the need for awareness of bone health in patients with epilepsy. The pathophysiological mechanisms are many and various wanting for further research in the less well-characterized areas. Furthermore, great responsibility rests on the healthcare professionals in implementing comprehensive patient care and in assuring bone protective measures in clinical practice to prevent bone loss in patients with epilepsy.

Original languageEnglish
Article number106511
JournalEpilepsy and Behavior
Volume100
Issue numberPart A
Number of pages10
ISSN1525-5050
DOIs
Publication statusPublished - Nov 2019

    Research areas

  • Antiepileptic drugs, Epilepsy, Fractures, Metabolic bone disease, Osteoporosis, Pathophysiology

ID: 239957929