title: Bone loss associated with use of antiepileptic drugs.
abstract: BACKGROUND
  Epilepsy is a neurological disorder associated with several comorbidities, one of them being reduced bone health. As the bone loss most often is insidious and asymptomatic, they are usually not recognized, and thus untreated. The key message of this paper is to make clinicians aware of the problem.
  
  
  METHODS
  This article reviews data from basic and clinical studies of bone loss associated with usage of antiepileptic drugs (AEDs) within the last 4 decades.
  
  
  RESULTS
  The reader will learn that there is accumulating evidence of biochemical abnormalities indicating a disturbed bone metabolism, a decreased bone density and a 2 - 6 times increased risk of fractures among those with epilepsy compared to the general population. These findings most likely have many causes, both internal and external, but long-term use of AEDs seems to play an important role. Enzyme-inducing drugs, such as phenytoin, phenobarbital and carbamazepine, but also the enzyme inhibitor valproate, appear to have bone-depleting properties. Reduced bone density may be detected during the first 1 - 5 years of treatment. Although many theories have been launched, the exact mechanisms by which the the drugs affect bone architecture are not fully understood.
  
  
  CONCLUSIONS
  We recommend clinicians to promote osteoprotective behavior among their epilepsy patients; that is, sunlight exposure and weight-bearing exercise as well as avoidance of risk factors such as bone-depleting drugs other than AEDs, smoking and heavy alcohol consumption. Enzyme inducing drugs should be avoided, if possible. Bone mineral density screening should be assessed on an individual basis, taking risk factors for bone loss into account. All patients taking AEDs on long-term basis ought to have adequate amounts of dietary calcium and vitamin D, and those who have developed bone loss should in addition be given specific antiosteoporotic treatment.
authors.affiliation: Oslo University Hospital, National Centre for Epilepsy, Division for Clinical Neuroscience, Section for Adult Epileptology, Department of Neurology, P.O. Box 53, 1306 Baerum Postterminal, G.F. Henriksens vei 23, Sandvika 1337, Oslo 0027, Norway. karl.otto.nakken@epilepsy.no
authors.forename: Karl O
authors.initials: KO
authors.lastname: Nakken
authors.forename: Erik
authors.initials: E
authors.lastname: Taubøll
mesh_terms: D000818:Animals; D000927:Anticonvulsants / Q000009:adverse effects* / Q000627:therapeutic use; D015519:Bone Density / Q000187:drug effects*; D001846:Bone Development / Q000187:drug effects; D001842:Bone and Bones / Q000378:metabolism / Q000503:physiopathology; D004827:Epilepsy / Q000188:drug therapy*; D050723:Fractures, Bone / Q000139:chemically induced; D006801:Humans; D010024:Osteoporosis / Q000139:chemically induced*
chemical_list: D000927:Anticonvulsants