Long-term treatment with raloxifene, but not bisphosphonates, reduces circulating sclerostin levels in postmenopausal women

Summary We determined whether suppression of sclerostin levels by estrogen treatment was mediated by anti-resorptive effect. Raloxifene, but not bisphosphonates, suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, indepen...

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Veröffentlicht in:Osteoporosis international 2012-04, Vol.23 (4), p.1235-1243
Hauptverfasser: Chung, Y. E., Lee, S. H., Lee, S.-Y., Kim, S.-Y., Kim, H.-H., Mirza, F. S., Lee, S.-K., Lorenzo, J. A., Kim, G. S., Koh, J.-M.
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container_end_page 1243
container_issue 4
container_start_page 1235
container_title Osteoporosis international
container_volume 23
creator Chung, Y. E.
Lee, S. H.
Lee, S.-Y.
Kim, S.-Y.
Kim, H.-H.
Mirza, F. S.
Lee, S.-K.
Lorenzo, J. A.
Kim, G. S.
Koh, J.-M.
description Summary We determined whether suppression of sclerostin levels by estrogen treatment was mediated by anti-resorptive effect. Raloxifene, but not bisphosphonates, suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects. Introduction Circulating sclerostin concentrations are higher in postmenopausal than in premenopausal women, and estrogen treatment suppresses sclerostin levels in both men and women. We determined whether anti-resorptives may suppress the circulating sclerostin levels. Methods We conducted a retrospective observational study. Eighty postmenopausal women were treated with raloxifene for 19.4 ± 7.7 months ( n  = 16), bisphosphonates for 19.2 ± 6.7 months ( n  = 32), or were untreated ( n  = 32) for 17.1 ± 4.6 months. Plasma sclerostin concentrations were measured before and after treatment. Results Plasma sclerostin levels after treatment were significantly lower in the raloxifene than in the control group (55.8 ± 23.4 pmol/l vs. 92.1 ± 50.4 pmol/l, p  = 0.046), but were similar between the bisphosphonate and control groups. Relative to baseline, raloxifene treatment markedly reduced plasma sclerostin concentration (−40.7 ± 22.8%, p  
doi_str_mv 10.1007/s00198-011-1675-1
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E. ; Lee, S. H. ; Lee, S.-Y. ; Kim, S.-Y. ; Kim, H.-H. ; Mirza, F. S. ; Lee, S.-K. ; Lorenzo, J. A. ; Kim, G. S. ; Koh, J.-M.</creator><creatorcontrib>Chung, Y. E. ; Lee, S. H. ; Lee, S.-Y. ; Kim, S.-Y. ; Kim, H.-H. ; Mirza, F. S. ; Lee, S.-K. ; Lorenzo, J. A. ; Kim, G. S. ; Koh, J.-M.</creatorcontrib><description>Summary We determined whether suppression of sclerostin levels by estrogen treatment was mediated by anti-resorptive effect. Raloxifene, but not bisphosphonates, suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects. Introduction Circulating sclerostin concentrations are higher in postmenopausal than in premenopausal women, and estrogen treatment suppresses sclerostin levels in both men and women. We determined whether anti-resorptives may suppress the circulating sclerostin levels. Methods We conducted a retrospective observational study. Eighty postmenopausal women were treated with raloxifene for 19.4 ± 7.7 months ( n  = 16), bisphosphonates for 19.2 ± 6.7 months ( n  = 32), or were untreated ( n  = 32) for 17.1 ± 4.6 months. Plasma sclerostin concentrations were measured before and after treatment. Results Plasma sclerostin levels after treatment were significantly lower in the raloxifene than in the control group (55.8 ± 23.4 pmol/l vs. 92.1 ± 50.4 pmol/l, p  = 0.046), but were similar between the bisphosphonate and control groups. Relative to baseline, raloxifene treatment markedly reduced plasma sclerostin concentration (−40.7 ± 22.8%, p  &lt; 0.001), with respect to both control (−7.5 ± 29.1%) and bisphosphonate (−3.1 ± 35.2%) groups. Changes in bone-specific alkaline phosphatase and osteocalcin levels showed reverse associations with sclerostin concentration changes in the raloxifene ( γ  = −0.505, p  = 0.017) and control ( γ  = −0.410, p  = 0.020) groups. Conclusions Raloxifene, but not bisphosphonates, significantly suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects.</description><identifier>ISSN: 0937-941X</identifier><identifier>EISSN: 1433-2965</identifier><identifier>DOI: 10.1007/s00198-011-1675-1</identifier><identifier>PMID: 21660558</identifier><language>eng</language><publisher>London: Springer-Verlag</publisher><subject>Aged ; Alkaline phosphatase ; Alkaline Phosphatase - blood ; Biomarkers - blood ; Bisphosphonates ; Bone Density - drug effects ; Bone Density Conservation Agents - administration &amp; dosage ; Bone Density Conservation Agents - pharmacology ; Bone Density Conservation Agents - therapeutic use ; Bone Morphogenetic Proteins - blood ; Bone Morphogenetic Proteins - drug effects ; Bone turnover ; Bones ; Diphosphonates - administration &amp; dosage ; Diphosphonates - pharmacology ; Diphosphonates - therapeutic use ; Drug Administration Schedule ; Drug therapy ; Endocrinology ; Estrogen receptors ; Estrogens ; Female ; Genetic Markers - drug effects ; Humans ; Medicine ; Medicine &amp; Public Health ; Menopause ; Metabolism ; Middle Aged ; Original Article ; Orthopedics ; Osteocalcin ; Osteocalcin - blood ; Osteoporosis ; Osteoporosis, Postmenopausal - blood ; Osteoporosis, Postmenopausal - drug therapy ; Osteoporosis, Postmenopausal - physiopathology ; Post-menopause ; Raloxifene ; Raloxifene Hydrochloride - administration &amp; dosage ; Raloxifene Hydrochloride - pharmacology ; Raloxifene Hydrochloride - therapeutic use ; Retrospective Studies ; Rheumatology ; Selective Estrogen Receptor Modulators - administration &amp; dosage ; Selective Estrogen Receptor Modulators - pharmacology ; Selective Estrogen Receptor Modulators - therapeutic use ; SOST protein</subject><ispartof>Osteoporosis international, 2012-04, Vol.23 (4), p.1235-1243</ispartof><rights>International Osteoporosis Foundation and National Osteoporosis Foundation 2011</rights><rights>International Osteoporosis Foundation and National Osteoporosis Foundation 2012</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c402t-ef81ccbac0e2753ffcdad596f56ba6c6bb75f3ca8a4a56687d39f2f3ad4da3063</citedby><cites>FETCH-LOGICAL-c402t-ef81ccbac0e2753ffcdad596f56ba6c6bb75f3ca8a4a56687d39f2f3ad4da3063</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00198-011-1675-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00198-011-1675-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21660558$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chung, Y. E.</creatorcontrib><creatorcontrib>Lee, S. H.</creatorcontrib><creatorcontrib>Lee, S.-Y.</creatorcontrib><creatorcontrib>Kim, S.-Y.</creatorcontrib><creatorcontrib>Kim, H.-H.</creatorcontrib><creatorcontrib>Mirza, F. S.</creatorcontrib><creatorcontrib>Lee, S.-K.</creatorcontrib><creatorcontrib>Lorenzo, J. A.</creatorcontrib><creatorcontrib>Kim, G. S.</creatorcontrib><creatorcontrib>Koh, J.-M.</creatorcontrib><title>Long-term treatment with raloxifene, but not bisphosphonates, reduces circulating sclerostin levels in postmenopausal women</title><title>Osteoporosis international</title><addtitle>Osteoporos Int</addtitle><addtitle>Osteoporos Int</addtitle><description>Summary We determined whether suppression of sclerostin levels by estrogen treatment was mediated by anti-resorptive effect. Raloxifene, but not bisphosphonates, suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects. Introduction Circulating sclerostin concentrations are higher in postmenopausal than in premenopausal women, and estrogen treatment suppresses sclerostin levels in both men and women. We determined whether anti-resorptives may suppress the circulating sclerostin levels. Methods We conducted a retrospective observational study. Eighty postmenopausal women were treated with raloxifene for 19.4 ± 7.7 months ( n  = 16), bisphosphonates for 19.2 ± 6.7 months ( n  = 32), or were untreated ( n  = 32) for 17.1 ± 4.6 months. Plasma sclerostin concentrations were measured before and after treatment. Results Plasma sclerostin levels after treatment were significantly lower in the raloxifene than in the control group (55.8 ± 23.4 pmol/l vs. 92.1 ± 50.4 pmol/l, p  = 0.046), but were similar between the bisphosphonate and control groups. Relative to baseline, raloxifene treatment markedly reduced plasma sclerostin concentration (−40.7 ± 22.8%, p  &lt; 0.001), with respect to both control (−7.5 ± 29.1%) and bisphosphonate (−3.1 ± 35.2%) groups. Changes in bone-specific alkaline phosphatase and osteocalcin levels showed reverse associations with sclerostin concentration changes in the raloxifene ( γ  = −0.505, p  = 0.017) and control ( γ  = −0.410, p  = 0.020) groups. Conclusions Raloxifene, but not bisphosphonates, significantly suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects.</description><subject>Aged</subject><subject>Alkaline phosphatase</subject><subject>Alkaline Phosphatase - blood</subject><subject>Biomarkers - blood</subject><subject>Bisphosphonates</subject><subject>Bone Density - drug effects</subject><subject>Bone Density Conservation Agents - administration &amp; dosage</subject><subject>Bone Density Conservation Agents - pharmacology</subject><subject>Bone Density Conservation Agents - therapeutic use</subject><subject>Bone Morphogenetic Proteins - blood</subject><subject>Bone Morphogenetic Proteins - drug effects</subject><subject>Bone turnover</subject><subject>Bones</subject><subject>Diphosphonates - administration &amp; dosage</subject><subject>Diphosphonates - pharmacology</subject><subject>Diphosphonates - therapeutic use</subject><subject>Drug Administration Schedule</subject><subject>Drug therapy</subject><subject>Endocrinology</subject><subject>Estrogen receptors</subject><subject>Estrogens</subject><subject>Female</subject><subject>Genetic Markers - drug effects</subject><subject>Humans</subject><subject>Medicine</subject><subject>Medicine &amp; Public Health</subject><subject>Menopause</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Original Article</subject><subject>Orthopedics</subject><subject>Osteocalcin</subject><subject>Osteocalcin - blood</subject><subject>Osteoporosis</subject><subject>Osteoporosis, Postmenopausal - blood</subject><subject>Osteoporosis, Postmenopausal - drug therapy</subject><subject>Osteoporosis, Postmenopausal - physiopathology</subject><subject>Post-menopause</subject><subject>Raloxifene</subject><subject>Raloxifene Hydrochloride - administration &amp; dosage</subject><subject>Raloxifene Hydrochloride - pharmacology</subject><subject>Raloxifene Hydrochloride - therapeutic use</subject><subject>Retrospective Studies</subject><subject>Rheumatology</subject><subject>Selective Estrogen Receptor Modulators - administration &amp; dosage</subject><subject>Selective Estrogen Receptor Modulators - pharmacology</subject><subject>Selective Estrogen Receptor Modulators - therapeutic use</subject><subject>SOST protein</subject><issn>0937-941X</issn><issn>1433-2965</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kUuPFCEUhYnROG3rD3BjiBs3g_IoqGJpJr6STtxo4o5Q1KWnJhSUQDka_7x0etTExAXhcvnO4ZKD0FNGXzJK-1eFUqYHQhkjTPWSsHtoxzohCNdK3kc7qkVPdMe-XKBHpdzQptG6f4guOFOKSjns0M9DikdSIS-4ZrB1gVjx7VyvcbYhfZ89RLjE41ZxTBWPc1mv02lFW6Fc4gzT5qBgN2e3BVvneMTFBciptBoH-Aah4FatrdG802q3YgO-Te3wGD3wNhR4crfv0ee3bz5dvSeHj-8-XL0-ENdRXgn4gTk3WkeB91J47yY7Sa28VKNVTo1jL71wdrCdlUoN_SS0517YqZusoErs0Yuz75rT1w1KNctcHIRgI6StGK0GNgiuaSOf_0PepC3HNpzRfKCs5w3cI3aGXPtlyeDNmufF5h-GUXPKxZxzMS0Xc8rFsKZ5dme8jQtMfxS_g2gAPwOlXcUj5L8v_9_1F5-QnHI</recordid><startdate>20120401</startdate><enddate>20120401</enddate><creator>Chung, Y. 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E.</creatorcontrib><creatorcontrib>Lee, S. H.</creatorcontrib><creatorcontrib>Lee, S.-Y.</creatorcontrib><creatorcontrib>Kim, S.-Y.</creatorcontrib><creatorcontrib>Kim, H.-H.</creatorcontrib><creatorcontrib>Mirza, F. S.</creatorcontrib><creatorcontrib>Lee, S.-K.</creatorcontrib><creatorcontrib>Lorenzo, J. A.</creatorcontrib><creatorcontrib>Kim, G. S.</creatorcontrib><creatorcontrib>Koh, J.-M.</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>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Nursing &amp; Allied Health Database</collection><collection>Physical Education Index</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</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</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Database (Alumni Edition)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing &amp; Allied Health Premium</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><jtitle>Osteoporosis international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chung, Y. E.</au><au>Lee, S. H.</au><au>Lee, S.-Y.</au><au>Kim, S.-Y.</au><au>Kim, H.-H.</au><au>Mirza, F. S.</au><au>Lee, S.-K.</au><au>Lorenzo, J. A.</au><au>Kim, G. S.</au><au>Koh, J.-M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long-term treatment with raloxifene, but not bisphosphonates, reduces circulating sclerostin levels in postmenopausal women</atitle><jtitle>Osteoporosis international</jtitle><stitle>Osteoporos Int</stitle><addtitle>Osteoporos Int</addtitle><date>2012-04-01</date><risdate>2012</risdate><volume>23</volume><issue>4</issue><spage>1235</spage><epage>1243</epage><pages>1235-1243</pages><issn>0937-941X</issn><eissn>1433-2965</eissn><abstract>Summary We determined whether suppression of sclerostin levels by estrogen treatment was mediated by anti-resorptive effect. Raloxifene, but not bisphosphonates, suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects. Introduction Circulating sclerostin concentrations are higher in postmenopausal than in premenopausal women, and estrogen treatment suppresses sclerostin levels in both men and women. We determined whether anti-resorptives may suppress the circulating sclerostin levels. Methods We conducted a retrospective observational study. Eighty postmenopausal women were treated with raloxifene for 19.4 ± 7.7 months ( n  = 16), bisphosphonates for 19.2 ± 6.7 months ( n  = 32), or were untreated ( n  = 32) for 17.1 ± 4.6 months. Plasma sclerostin concentrations were measured before and after treatment. Results Plasma sclerostin levels after treatment were significantly lower in the raloxifene than in the control group (55.8 ± 23.4 pmol/l vs. 92.1 ± 50.4 pmol/l, p  = 0.046), but were similar between the bisphosphonate and control groups. Relative to baseline, raloxifene treatment markedly reduced plasma sclerostin concentration (−40.7 ± 22.8%, p  &lt; 0.001), with respect to both control (−7.5 ± 29.1%) and bisphosphonate (−3.1 ± 35.2%) groups. Changes in bone-specific alkaline phosphatase and osteocalcin levels showed reverse associations with sclerostin concentration changes in the raloxifene ( γ  = −0.505, p  = 0.017) and control ( γ  = −0.410, p  = 0.020) groups. Conclusions Raloxifene, but not bisphosphonates, significantly suppressed circulating sclerostin concentration, suggesting that sclerostin may mediate the action of estrogen on bone metabolism, independently of their anti-resorptive effects.</abstract><cop>London</cop><pub>Springer-Verlag</pub><pmid>21660558</pmid><doi>10.1007/s00198-011-1675-1</doi><tpages>9</tpages></addata></record>
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subjects Aged
Alkaline phosphatase
Alkaline Phosphatase - blood
Biomarkers - blood
Bisphosphonates
Bone Density - drug effects
Bone Density Conservation Agents - administration & dosage
Bone Density Conservation Agents - pharmacology
Bone Density Conservation Agents - therapeutic use
Bone Morphogenetic Proteins - blood
Bone Morphogenetic Proteins - drug effects
Bone turnover
Bones
Diphosphonates - administration & dosage
Diphosphonates - pharmacology
Diphosphonates - therapeutic use
Drug Administration Schedule
Drug therapy
Endocrinology
Estrogen receptors
Estrogens
Female
Genetic Markers - drug effects
Humans
Medicine
Medicine & Public Health
Menopause
Metabolism
Middle Aged
Original Article
Orthopedics
Osteocalcin
Osteocalcin - blood
Osteoporosis
Osteoporosis, Postmenopausal - blood
Osteoporosis, Postmenopausal - drug therapy
Osteoporosis, Postmenopausal - physiopathology
Post-menopause
Raloxifene
Raloxifene Hydrochloride - administration & dosage
Raloxifene Hydrochloride - pharmacology
Raloxifene Hydrochloride - therapeutic use
Retrospective Studies
Rheumatology
Selective Estrogen Receptor Modulators - administration & dosage
Selective Estrogen Receptor Modulators - pharmacology
Selective Estrogen Receptor Modulators - therapeutic use
SOST protein
title Long-term treatment with raloxifene, but not bisphosphonates, reduces circulating sclerostin levels in postmenopausal women
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