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Commentary Persons with epilepsy have a twoto six-fold increased risk of fracture (1). Antiepileptic drug (AED) exposure independently increases the risk (2, 3). Therefore, when choosing an AED, it is important to understand its potential secondary effects on bone. AEDs most commonly associated with adverse effects on bone include phenytoin and phenobarbital (1). Levetiracetam is a broad-spectrum AED used for the treatment of partial and generalized epilepsy syndromes. Whether levetiracetam affects bone has received limited study and is not well understood. The impact of levetiracetam on bone was previously evaluated in an animal study (4). Rats were treated with low-dose (50 mg/kg) and high-dose (150 mg/kg) levetiracetam. Levetiracetam did not affect bone mass. Low-dose levetiracetam was associated with reduced biochemical strength of the femoral neck, which is predominantly trabecular bone. Trabecular bone is metabolically active bone and contains relatively more cartilage. The femoral diaphysis, which is predominantly cortical bone was not significantly altered. In addition, osteocalcin, a marker of bone formation, was increased in low-dose levetiracetam–treated animals. Increased osteocalcin reflects increased bone turnover resulting in bone loss over time. An abstract presentation of 16 subjects showed a favorable effect of levetiracetam on bone mineral density (BMD) and vitamin D concentrations (5). Subjects ranging in age from 20 to 66 had BMD measurements using dual energy x-ray absorptiometry (DXA) and serologic vitamin D concentrations as well as osteocalcin measurements after a minimum of 6 months levetiracetam exposure. DXA is the most commonly used tool to assess BMD. No subject had evidence of low bone mass (osteopenia or osteoporosis). Osteopenia is defined by the World Health Organization as T-scores between −1.0 and −2.5. Osteoporosis is defined as −2.5 or lower. All subjects had vitamin D concentrations in the normal range. Four subjects had elevated osteocalcin. In the absence of other bone turnover markers, and normal BMD, this finding is of unclear significance. Unfortunately, these results were never published as a peer-reviewed paper. In contrast, a retrospective cross-sectional study, published as a short communication, found that the incidence of low BMD (either osteopenia or osteoporosis) was higher among levetiracetam monotherapy users compared with users of other AEDs including topiramate, lamotrigine, carbamazepine, and valproate (6). Among 17 subjects treated with levetiracetam, 70% had low BMD. This study is limited by the sample size and lack of evaluation of potential confounders such as diet and exercise. In order to better understand the effects of levetiracetam on bone, Koo and colleagues designed a prospective study evaluating BMD and bone metabolism among drug-naïve subjects (average age 31.0 ± 13.1 years) with recent onset epilepsy treated with levetiracetam monotherapy (mean duration 14.16 ± 3.36 months) (7). Subjects were recruited from a Korean outpatient epilepsy clinic; among the original 107 Effects of Levetiracetam as a Monotherapy on Bone Mineral Density and Biochemical Markers of Bone Metabolism in Patients With Epilepsy.

Levetiracetam Treatment Does Not Result in Broken Bones