Bone disease in epilepsy

Abstract

Recent literature demonstrates an association between antiepileptic drugs (AEDs) and bone disease. Decreased bone mineral density (BMD) has been found in adults and children receiving both enzyme-inducing AEDs and valproate, which is an enzyme-inhibiting AED. Biochemical abnormalities include hypocalcemia, elevated parathyroid hormone, and elevated markers of bone formation and resorption. Although patients in earlier studies had evidence of decreased vitamin D, low BMD has been found to be independent of abnormal vitamin D chemistries in more recently published studies. Multiple mechanisms have been postulated to explain AED-associated bone disease, but no single mechanism fully explains all the abnormalities seen. Therapies are available for bone disease. However, few studies have evaluated the effects of treatment in bone disease associated with AEDs.

Symptomatic hypocalcemia in an epileptic child treated with valproic acid plus lamotrigine: a case report

“…Anticonvulsant drugs have hypocalcemic effects [1-5], with mechanism that differ depending upon the class of drugs considered. The inductors of the P450 cytochrome enzymes diphenylhydantoin, carbamazepine, pyridostigmine are known to enhance vitamin D catabolism, with a consequent reduction of its biological effects.…”

“…phenobarbital, phenytoine, carbamazepine, primidone), more recent studies highlight the possible involvement of other anticonvulsant drugs, such as valproic acid. The mechanism involved in such alteration is still matter of open debate [1,2]. …”

The pathogenesis of tibial non-union

“…Phenytoin, phenobarbital, carbamazepine primidone and valproate have all been implicated in causing decreased bone mineral density and disorders of bone metabolism. [87][88][89][90][91] The extent to which these drugs affect fracture healing in humans remains to be evaluated.…”

Effekte von Carbamazepin und Oxcarbazepin auf den Knochenstoffwechsel

“…Antikonvulsiva-assoziierte Knochenstoffwechselstörungen lassen sich somit nicht allein auf enzyminduzierende Mechanismen zurückführen [1,9,21]. Für Phenytoin und Carbamazepin konnten auch direkte inhibitorische Effekte auf Osteoblasten nachgewiesen werden.…”