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    Glucocorticoid-Induced Bone Loss Is Associated with Abnormal Intravertebral Areal Bone Mineral Density Distribution

    191660_191660.pdf (2.112Mb)
    Access Status
    Open access
    Authors
    Manning, Louise
    Briggs, Andrew
    Van Doornum, Sharon
    Kale, Ashwini
    Kantor, Susan
    Wark, John
    Date
    2013
    Type
    Journal Article
    
    Metadata
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    Citation
    Manning, Louise and Briggs, Andrew and Van Doornum, Sharon and Kale, Ashwini and Kantor, Susan and Wark, John. 2013. Glucocorticoid-Induced Bone Loss Is Associated with Abnormal Intravertebral Areal Bone Mineral Density Distribution. International Journal of Endocrinology. Article ID 768579: 9 pages.
    Source Title
    International Journal of Endocrinology
    DOI
    10.1155/2013/768579
    ISSN
    1687-8345
    Remarks

    This article is published under the Open Access publishing model and distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/ Please refer to the licence to obtain terms for any further reuse or distribution of this work.

    Copyright © 2013 Louise I. Manning et al.

    URI
    http://hdl.handle.net/20.500.11937/46126
    Collection
    • Curtin Research Publications
    Abstract

    Individuals with glucocorticoid-induced osteoporosis experience vertebral fractures at an increased rate and at higher vertebral areal bone mineral density (aBMD) than individuals with primary osteoporosis. Standard posteroanterior- (PA-) projection dual energy X-ray absorptiometry (DXA) lacks the diagnostic sensitivity required for reliable estimation of vertebral fracture risk in individuals. Assessment of subregional vertebral aBMD using lateral-projection DXA may improve the predictive value of DXA parameters for fracture. One hundred and four individuals were recruited and grouped for this study: primary osteoporosis with no history of vertebral fracture (n = 43), glucocorticoid-induced bone loss (n = 13), and healthy controls (n = 48). Standard PA-projection and supine-lateral scans were performed, and lateral scans were analysed according to an established protocol to measure aBMD within 6 subregions. Main effects for subregion and group were assessed and observed, by ANCOVA. Ratios were calculated between subregions and compared between groups, to overcome the potentially confounding influence of variability in subregional geometry. Significantly lower values were observed in the glucocorticoid group for the ratios of (i) anterior subregion: whole vertebral body and (ii) posterior: whole vertebral body when compared to the primary osteoporosis and control groups (P < 0.0 5). Lower anterior subregional aBMD in individuals on glucocorticoid therapy may help to explain the increased vertebral fracture risk in this patient group.

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