SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength

Objective The objective of this report is to assess the effect of systemic lupus erythematosus (SLE) disease itself on deterioration of bone mineral density (BMD), microstructure and bone strength. Method Thirty age-matched SLE patients on long-term glucocorticoids (GC) (SLE/GC), 30 SLE patients wit...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Lupus 2013-10, Vol.22 (11), p.1162-1168
Hauptverfasser: Tang, XL, Griffith, JF, Qin, L, Hung, VW, Kwok, AW, Zhu, TY, Kun, EW, Leung, PC, Li, EK, Tam, L-S
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 1168
container_issue 11
container_start_page 1162
container_title Lupus
container_volume 22
creator Tang, XL
Griffith, JF
Qin, L
Hung, VW
Kwok, AW
Zhu, TY
Kun, EW
Leung, PC
Li, EK
Tam, L-S
description Objective The objective of this report is to assess the effect of systemic lupus erythematosus (SLE) disease itself on deterioration of bone mineral density (BMD), microstructure and bone strength. Method Thirty age-matched SLE patients on long-term glucocorticoids (GC) (SLE/GC), 30 SLE patients without GC (SLE/non-GC) and 60 healthy controls were examined. Areal BMD (aBMD) was measured by dual-energy X-ray absorptiometry. Bone geometry, volumetric BMD (vBMD), and architectural parameters at the nondominant distal radius were assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT). Bone strength was estimated by HR-pQCT-based micro-finite element analysis. Results Adjusted for menopausal status and adjusted calcium level, when compared with controls, SLE/non-GC patients had significantly lower aBMD at femoral neck and total hip, and diminished radial total vBMD, cortical area, vBMD and thickness, respectively, by 8.3%, 8%, 2.7% and 9.2%, as well as significant compromised bone strength (stiffness, failure load and apparent modulus) by 8.3%, 9.1% and 9.5%, respectively. Similar alterations were also found in SLE/GC patients when compared to controls. In the premenopausal subgroup analysis, when compared with controls, total hip aBMD and radial cortical area were significantly lower in SLE/non-GC patients, and cortical area and thickness were significantly deficit in SLE/GC patients. However, no significant difference in any bone variables was present between SLE/GC and SLE/non-GC patients in the entire cohort or in the premenopausal subgroup. Conclusion SLE disease per se contributes to the deterioration in bone density, cortical microstructure and bone strength. This might help to explain the considerably higher fracture risk seen in SLE patients.
doi_str_mv 10.1177/0961203313498802
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1435845910</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_0961203313498802</sage_id><sourcerecordid>1435845910</sourcerecordid><originalsourceid>FETCH-LOGICAL-c431t-95382a8c4540642fae6de05c9ad8af302c3ccf6d6d8ea797026d2dacc6faf1623</originalsourceid><addsrcrecordid>eNp1kUtLAzEUhYMotj72riTgxoWjecwkmaWILyi4UNdDmtypKW1Sk8zCf29qVaTg6sI53zl5XIROKLmkVMor0grKCOeU161ShO2gMa2lrIrOdtF4bVdrf4QOUpoTQjhtxT4aMa5USYgxcs-TW2xdAp0AryDiMkzwObrpkCHhHLCFDNGFqLMLHjuPp8EDXjoPUS-K65PLHxdFMDGkHAeThwhYe7sBiwR-lt-O0F6vFwmOv-cher27fbl5qCZP948315PK1Jzmqm24YlqZuqmJqFmvQVggjWm1VbrnhBluTC-ssAq0bCVhwjKrjRG97qlg_BCdb3pXMbwPkHK3dMnAYqE9hCF1tOaNqpuWkoKebaHzMERfbvdFtVLKr0KyodbvSxH6bhXdUsePjpJuvYZuew0lcvpdPEyXYH8DP_9egGoDJD2DP6f-V_gJ0PqQJw</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1435977762</pqid></control><display><type>article</type><title>SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength</title><source>MEDLINE</source><source>SAGE Complete A-Z List</source><creator>Tang, XL ; Griffith, JF ; Qin, L ; Hung, VW ; Kwok, AW ; Zhu, TY ; Kun, EW ; Leung, PC ; Li, EK ; Tam, L-S</creator><creatorcontrib>Tang, XL ; Griffith, JF ; Qin, L ; Hung, VW ; Kwok, AW ; Zhu, TY ; Kun, EW ; Leung, PC ; Li, EK ; Tam, L-S</creatorcontrib><description>Objective The objective of this report is to assess the effect of systemic lupus erythematosus (SLE) disease itself on deterioration of bone mineral density (BMD), microstructure and bone strength. Method Thirty age-matched SLE patients on long-term glucocorticoids (GC) (SLE/GC), 30 SLE patients without GC (SLE/non-GC) and 60 healthy controls were examined. Areal BMD (aBMD) was measured by dual-energy X-ray absorptiometry. Bone geometry, volumetric BMD (vBMD), and architectural parameters at the nondominant distal radius were assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT). Bone strength was estimated by HR-pQCT-based micro-finite element analysis. Results Adjusted for menopausal status and adjusted calcium level, when compared with controls, SLE/non-GC patients had significantly lower aBMD at femoral neck and total hip, and diminished radial total vBMD, cortical area, vBMD and thickness, respectively, by 8.3%, 8%, 2.7% and 9.2%, as well as significant compromised bone strength (stiffness, failure load and apparent modulus) by 8.3%, 9.1% and 9.5%, respectively. Similar alterations were also found in SLE/GC patients when compared to controls. In the premenopausal subgroup analysis, when compared with controls, total hip aBMD and radial cortical area were significantly lower in SLE/non-GC patients, and cortical area and thickness were significantly deficit in SLE/GC patients. However, no significant difference in any bone variables was present between SLE/GC and SLE/non-GC patients in the entire cohort or in the premenopausal subgroup. Conclusion SLE disease per se contributes to the deterioration in bone density, cortical microstructure and bone strength. This might help to explain the considerably higher fracture risk seen in SLE patients.</description><identifier>ISSN: 0961-2033</identifier><identifier>EISSN: 1477-0962</identifier><identifier>DOI: 10.1177/0961203313498802</identifier><identifier>PMID: 23884986</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Adult ; Bone and Bones - pathology ; Bone and Bones - physiopathology ; Bone Density ; Female ; Fractures ; Geometry ; Glucocorticoids - therapeutic use ; Humans ; Lupus ; Lupus Erythematosus, Systemic - complications ; Lupus Erythematosus, Systemic - drug therapy ; Lupus Erythematosus, Systemic - pathology ; Lupus Erythematosus, Systemic - physiopathology ; Middle Aged ; Tomography ; Tomography, X-Ray Computed ; Variance analysis</subject><ispartof>Lupus, 2013-10, Vol.22 (11), p.1162-1168</ispartof><rights>The Author(s) 2013 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav</rights><rights>SAGE Publications © Oct 2013</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c431t-95382a8c4540642fae6de05c9ad8af302c3ccf6d6d8ea797026d2dacc6faf1623</citedby><cites>FETCH-LOGICAL-c431t-95382a8c4540642fae6de05c9ad8af302c3ccf6d6d8ea797026d2dacc6faf1623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/0961203313498802$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1177/0961203313498802$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,777,781,21800,27905,27906,43602,43603</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23884986$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tang, XL</creatorcontrib><creatorcontrib>Griffith, JF</creatorcontrib><creatorcontrib>Qin, L</creatorcontrib><creatorcontrib>Hung, VW</creatorcontrib><creatorcontrib>Kwok, AW</creatorcontrib><creatorcontrib>Zhu, TY</creatorcontrib><creatorcontrib>Kun, EW</creatorcontrib><creatorcontrib>Leung, PC</creatorcontrib><creatorcontrib>Li, EK</creatorcontrib><creatorcontrib>Tam, L-S</creatorcontrib><title>SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength</title><title>Lupus</title><addtitle>Lupus</addtitle><description>Objective The objective of this report is to assess the effect of systemic lupus erythematosus (SLE) disease itself on deterioration of bone mineral density (BMD), microstructure and bone strength. Method Thirty age-matched SLE patients on long-term glucocorticoids (GC) (SLE/GC), 30 SLE patients without GC (SLE/non-GC) and 60 healthy controls were examined. Areal BMD (aBMD) was measured by dual-energy X-ray absorptiometry. Bone geometry, volumetric BMD (vBMD), and architectural parameters at the nondominant distal radius were assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT). Bone strength was estimated by HR-pQCT-based micro-finite element analysis. Results Adjusted for menopausal status and adjusted calcium level, when compared with controls, SLE/non-GC patients had significantly lower aBMD at femoral neck and total hip, and diminished radial total vBMD, cortical area, vBMD and thickness, respectively, by 8.3%, 8%, 2.7% and 9.2%, as well as significant compromised bone strength (stiffness, failure load and apparent modulus) by 8.3%, 9.1% and 9.5%, respectively. Similar alterations were also found in SLE/GC patients when compared to controls. In the premenopausal subgroup analysis, when compared with controls, total hip aBMD and radial cortical area were significantly lower in SLE/non-GC patients, and cortical area and thickness were significantly deficit in SLE/GC patients. However, no significant difference in any bone variables was present between SLE/GC and SLE/non-GC patients in the entire cohort or in the premenopausal subgroup. Conclusion SLE disease per se contributes to the deterioration in bone density, cortical microstructure and bone strength. This might help to explain the considerably higher fracture risk seen in SLE patients.</description><subject>Adult</subject><subject>Bone and Bones - pathology</subject><subject>Bone and Bones - physiopathology</subject><subject>Bone Density</subject><subject>Female</subject><subject>Fractures</subject><subject>Geometry</subject><subject>Glucocorticoids - therapeutic use</subject><subject>Humans</subject><subject>Lupus</subject><subject>Lupus Erythematosus, Systemic - complications</subject><subject>Lupus Erythematosus, Systemic - drug therapy</subject><subject>Lupus Erythematosus, Systemic - pathology</subject><subject>Lupus Erythematosus, Systemic - physiopathology</subject><subject>Middle Aged</subject><subject>Tomography</subject><subject>Tomography, X-Ray Computed</subject><subject>Variance analysis</subject><issn>0961-2033</issn><issn>1477-0962</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kUtLAzEUhYMotj72riTgxoWjecwkmaWILyi4UNdDmtypKW1Sk8zCf29qVaTg6sI53zl5XIROKLmkVMor0grKCOeU161ShO2gMa2lrIrOdtF4bVdrf4QOUpoTQjhtxT4aMa5USYgxcs-TW2xdAp0AryDiMkzwObrpkCHhHLCFDNGFqLMLHjuPp8EDXjoPUS-K65PLHxdFMDGkHAeThwhYe7sBiwR-lt-O0F6vFwmOv-cher27fbl5qCZP948315PK1Jzmqm24YlqZuqmJqFmvQVggjWm1VbrnhBluTC-ssAq0bCVhwjKrjRG97qlg_BCdb3pXMbwPkHK3dMnAYqE9hCF1tOaNqpuWkoKebaHzMERfbvdFtVLKr0KyodbvSxH6bhXdUsePjpJuvYZuew0lcvpdPEyXYH8DP_9egGoDJD2DP6f-V_gJ0PqQJw</recordid><startdate>20131001</startdate><enddate>20131001</enddate><creator>Tang, XL</creator><creator>Griffith, JF</creator><creator>Qin, L</creator><creator>Hung, VW</creator><creator>Kwok, AW</creator><creator>Zhu, TY</creator><creator>Kun, EW</creator><creator>Leung, PC</creator><creator>Li, EK</creator><creator>Tam, L-S</creator><general>SAGE Publications</general><general>Sage Publications Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9-</scope><scope>K9.</scope><scope>M0R</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20131001</creationdate><title>SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength</title><author>Tang, XL ; Griffith, JF ; Qin, L ; Hung, VW ; Kwok, AW ; Zhu, TY ; Kun, EW ; Leung, PC ; Li, EK ; Tam, L-S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c431t-95382a8c4540642fae6de05c9ad8af302c3ccf6d6d8ea797026d2dacc6faf1623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adult</topic><topic>Bone and Bones - pathology</topic><topic>Bone and Bones - physiopathology</topic><topic>Bone Density</topic><topic>Female</topic><topic>Fractures</topic><topic>Geometry</topic><topic>Glucocorticoids - therapeutic use</topic><topic>Humans</topic><topic>Lupus</topic><topic>Lupus Erythematosus, Systemic - complications</topic><topic>Lupus Erythematosus, Systemic - drug therapy</topic><topic>Lupus Erythematosus, Systemic - pathology</topic><topic>Lupus Erythematosus, Systemic - physiopathology</topic><topic>Middle Aged</topic><topic>Tomography</topic><topic>Tomography, X-Ray Computed</topic><topic>Variance analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tang, XL</creatorcontrib><creatorcontrib>Griffith, JF</creatorcontrib><creatorcontrib>Qin, L</creatorcontrib><creatorcontrib>Hung, VW</creatorcontrib><creatorcontrib>Kwok, AW</creatorcontrib><creatorcontrib>Zhu, TY</creatorcontrib><creatorcontrib>Kun, EW</creatorcontrib><creatorcontrib>Leung, PC</creatorcontrib><creatorcontrib>Li, EK</creatorcontrib><creatorcontrib>Tam, L-S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Consumer Health Database</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Lupus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tang, XL</au><au>Griffith, JF</au><au>Qin, L</au><au>Hung, VW</au><au>Kwok, AW</au><au>Zhu, TY</au><au>Kun, EW</au><au>Leung, PC</au><au>Li, EK</au><au>Tam, L-S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength</atitle><jtitle>Lupus</jtitle><addtitle>Lupus</addtitle><date>2013-10-01</date><risdate>2013</risdate><volume>22</volume><issue>11</issue><spage>1162</spage><epage>1168</epage><pages>1162-1168</pages><issn>0961-2033</issn><eissn>1477-0962</eissn><abstract>Objective The objective of this report is to assess the effect of systemic lupus erythematosus (SLE) disease itself on deterioration of bone mineral density (BMD), microstructure and bone strength. Method Thirty age-matched SLE patients on long-term glucocorticoids (GC) (SLE/GC), 30 SLE patients without GC (SLE/non-GC) and 60 healthy controls were examined. Areal BMD (aBMD) was measured by dual-energy X-ray absorptiometry. Bone geometry, volumetric BMD (vBMD), and architectural parameters at the nondominant distal radius were assessed by high-resolution peripheral quantitative computed tomography (HR-pQCT). Bone strength was estimated by HR-pQCT-based micro-finite element analysis. Results Adjusted for menopausal status and adjusted calcium level, when compared with controls, SLE/non-GC patients had significantly lower aBMD at femoral neck and total hip, and diminished radial total vBMD, cortical area, vBMD and thickness, respectively, by 8.3%, 8%, 2.7% and 9.2%, as well as significant compromised bone strength (stiffness, failure load and apparent modulus) by 8.3%, 9.1% and 9.5%, respectively. Similar alterations were also found in SLE/GC patients when compared to controls. In the premenopausal subgroup analysis, when compared with controls, total hip aBMD and radial cortical area were significantly lower in SLE/non-GC patients, and cortical area and thickness were significantly deficit in SLE/GC patients. However, no significant difference in any bone variables was present between SLE/GC and SLE/non-GC patients in the entire cohort or in the premenopausal subgroup. Conclusion SLE disease per se contributes to the deterioration in bone density, cortical microstructure and bone strength. This might help to explain the considerably higher fracture risk seen in SLE patients.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>23884986</pmid><doi>10.1177/0961203313498802</doi><tpages>7</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0961-2033
ispartof Lupus, 2013-10, Vol.22 (11), p.1162-1168
issn 0961-2033
1477-0962
language eng
recordid cdi_proquest_miscellaneous_1435845910
source MEDLINE; SAGE Complete A-Z List
subjects Adult
Bone and Bones - pathology
Bone and Bones - physiopathology
Bone Density
Female
Fractures
Geometry
Glucocorticoids - therapeutic use
Humans
Lupus
Lupus Erythematosus, Systemic - complications
Lupus Erythematosus, Systemic - drug therapy
Lupus Erythematosus, Systemic - pathology
Lupus Erythematosus, Systemic - physiopathology
Middle Aged
Tomography
Tomography, X-Ray Computed
Variance analysis
title SLE disease per se contributes to deterioration in bone mineral density, microstructure and bone strength
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T11%3A32%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=SLE%20disease%20per%20se%20contributes%20to%20deterioration%20in%20bone%20mineral%20density,%20microstructure%20and%20bone%20strength&rft.jtitle=Lupus&rft.au=Tang,%20XL&rft.date=2013-10-01&rft.volume=22&rft.issue=11&rft.spage=1162&rft.epage=1168&rft.pages=1162-1168&rft.issn=0961-2033&rft.eissn=1477-0962&rft_id=info:doi/10.1177/0961203313498802&rft_dat=%3Cproquest_cross%3E1435845910%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1435977762&rft_id=info:pmid/23884986&rft_sage_id=10.1177_0961203313498802&rfr_iscdi=true