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    Bone loss with antiepileptic drug therapy: a twin and sibling study

    Access Status
    Fulltext not available
    Authors
    Shiek Ahmad, B.
    Petty, S.
    Gorelik, A.
    O Brien, T.
    Hill, Keith
    Christie, J.
    Sambrook, P.
    Wark, J.
    Date
    2017
    Type
    Journal Article
    
    Metadata
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    Citation
    Shiek Ahmad, B. and Petty, S. and Gorelik, A. and O Brien, T. and Hill, K. and Christie, J. and Sambrook, P. et al. 2017. Bone loss with antiepileptic drug therapy: a twin and sibling study. Osteoporosis International: pp. 1-10.
    Source Title
    Osteoporosis International
    DOI
    10.1007/s00198-017-4098-9
    ISSN
    0937-941X
    School
    School of Physiotherapy and Exercise Science
    URI
    http://hdl.handle.net/20.500.11937/54859
    Collection
    • Curtin Research Publications
    Abstract

    © 2017 International Osteoporosis Foundation and National Osteoporosis FoundationSummary: Changes in areal bone mineral density (aBMD) and other predictors of bone loss were evaluated in 48 same-sex twin/age-matched sibling pairs discordant for antiepileptic drug (AED) use. AED users had reduced BMD at the hip regions. Prolonged AED users had greater aBMD loss, predicting a higher risk of bone fragility. Introduction: To investigate the longitudinal associations of bone mineral measures with antiepileptic drug (AED) use, including enzyme-inducing (EIAED) and non-enzyme-inducing (NEIAED) types, and other predictors of bone loss in a study of 48 same-sex twin/age-matched sibling pairs (40 female, 8 male) discordant for AED use. Methods: Using dual-energy X-ray absorptiometry (DXA), areal bone mineral density (aBMD) and content (BMC) at the hip regions, forearm, lumbar spine, and whole body were measured twice, at least 2 years apart. The mean within-pair difference (MWPD), MWPD%, and mean annual rate of aBMD change were adjusted for age, weight, and height. Predictors of bone loss were evaluated. Results: AED users, compared to non-users, at baseline and follow-up, respectively, had reduced aBMD at the total hip (MWPD% 3.8, 4.4%), femoral neck (4.7, 4.5%), and trochanter regions (4.1, 4.6%) (p < 0.05). For the whole cohort, the annual rate of change in all aBMD/BMC (p > 0.05) regions did not differ within pairs. Nevertheless, EIAED users had greater aBMD loss than non-users (n = 20 pairs) at the total hip (1.7 vs. 0.3%, p = 0.013) and whole body regions (0.7% loss vs. 0.1% BMD gain, p = 0.019), which was not found in NEIAED-discordant pairs (n = 16). AED use >20 years predicted higher aBMD loss at the forearm (p = 0.028), whole body (p = 0.010), and whole body BMC (p = 0.031). Conclusions: AED users had reduced aBMD at the hip regions. Prolonged users and EIAED users had greater aBMD loss, predicting a higher risk of bone fragility. Further prospective studies of AED effects on bone microarchitecture are needed.

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