Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate
Identifieur interne : 001469 ( PascalFrancis/Corpus ); précédent : 001468; suivant : 001470Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate
Auteurs : Philip N. Sambrook ; Christian Roux ; Jean-Pierre Devogelaer ; Kenneth Saag ; Chak-Sing Lau ; Jean-Yves Reginster ; Christina Bucci-Rechtweg ; GUOQIN SU ; David M. ReidSource :
- Bone : (New York, NY) [ 8756-3282 ] ; 2012.
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English descriptors
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Abstract
Background: We studied 265 men (mean age 56.4 years; range 18-83 years), among patients enrolled in two arms of a double-blind, 1-year study comparing the effects of zoledronic acid (ZOL) with risedronate (RIS) in patients either commencing (prednisolone 7.5 mg/day or equivalent) (prevention arm, n = 88) or continuing glucocorticoid therapy (treatment arm, n = 177). Methods: Patients received either a single ZOL 5 mg infusion or RIS 5 mg oral daily at randomization, along with calcium (1000 mg) and vitamin D (400-1200 IU). Primary endpoint: difference in percentage change from baseline in bone mineral density (BMD) at the lumbar spine (LS) at 12 months. Secondary endpoints: percentage changes in BMD at total hip (TH) and femoral neck (FN), relative changes in bone turnover markers (β-CTx and P1NP), and overall safety. Findings: In the treatment subpopulation, ZOL increased LS BMD by 4.7% vs. 3.3% for RIS and at TH the percentage changes were 1.8% vs. 0.2%, respectively. In the prevention subpopulation, bone loss was prevented by both treatments. At LS the percentage changes were 2.5% vs. - 0.2% for ZOL vs. RIS and at TH the percentage changes were 1.1% vs. -0.4%, respectively. ZOL significantly increased lumbar spine BMD more than RIS at Month 12 in both the prevention population (p=0.0024) and the treatment subpopulation (p = 0.0232) in men. In the treatment subpopulation, ZOL demonstrated a significantly greater reduction in serum β-CTx and P1NP relative to RIS at all time-points. In the prevention subpopulation, ZOL significantly reduced β-CTx at all time-points, and P1NP at Month 3 (p = 0.0297) only. Both treatments were well tolerated in men, albeit with a higher incidence of influenza-like illness and pyrexia events post-infusion with ZOL. Interpretation: Once-yearly ZOL preserves or increases BMD within 1 year to a greater extent than daily RIS in men receiving glucocorticoid therapy.
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Format Inist (serveur)
| NO : | PASCAL 12-0182339 INIST |
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| ET : | Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate |
| AU : | SAMBROOK (Philip N.); ROUX (Christian); DEVOGELAER (Jean-Pierre); SAAG (Kenneth); LAU (Chak-Sing); REGINSTER (Jean-Yves); BUCCI-RECHTWEG (Christina); GUOQIN SU; REID (David M.) |
| AF : | University of Sydney/Sydney, NSW/Australie (1 aut.); Paris-Descartes University/Paris/France (2 aut.); Université Catholique de Louvain at Brussels/Brussels/Belgique (3 aut.); University of Alabama at Birmingham/Birmingham, AL/Etats-Unis (4 aut.); University of Dundee/Dundee/Royaume-Uni (5 aut.); University of Liège/Liège/Belgique (6 aut.); Novartis Pharmaceuticals Corporation/East Hanover, NJ/Etats-Unis (7 aut., 8 aut.); University of Aberdeen/Aberdeen/Royaume-Uni (9 aut.) |
| DT : | Publication en série; Niveau analytique |
| SO : | Bone : (New York, NY); ISSN 8756-3282; Pays-Bas; Da. 2012; Vol. 50; No. 1; Pp. 289-295; Bibl. 42 ref. |
| LA : | Anglais |
| EA : | Background: We studied 265 men (mean age 56.4 years; range 18-83 years), among patients enrolled in two arms of a double-blind, 1-year study comparing the effects of zoledronic acid (ZOL) with risedronate (RIS) in patients either commencing (prednisolone 7.5 mg/day or equivalent) (prevention arm, n = 88) or continuing glucocorticoid therapy (treatment arm, n = 177). Methods: Patients received either a single ZOL 5 mg infusion or RIS 5 mg oral daily at randomization, along with calcium (1000 mg) and vitamin D (400-1200 IU). Primary endpoint: difference in percentage change from baseline in bone mineral density (BMD) at the lumbar spine (LS) at 12 months. Secondary endpoints: percentage changes in BMD at total hip (TH) and femoral neck (FN), relative changes in bone turnover markers (β-CTx and P1NP), and overall safety. Findings: In the treatment subpopulation, ZOL increased LS BMD by 4.7% vs. 3.3% for RIS and at TH the percentage changes were 1.8% vs. 0.2%, respectively. In the prevention subpopulation, bone loss was prevented by both treatments. At LS the percentage changes were 2.5% vs. - 0.2% for ZOL vs. RIS and at TH the percentage changes were 1.1% vs. -0.4%, respectively. ZOL significantly increased lumbar spine BMD more than RIS at Month 12 in both the prevention population (p=0.0024) and the treatment subpopulation (p = 0.0232) in men. In the treatment subpopulation, ZOL demonstrated a significantly greater reduction in serum β-CTx and P1NP relative to RIS at all time-points. In the prevention subpopulation, ZOL significantly reduced β-CTx at all time-points, and P1NP at Month 3 (p = 0.0297) only. Both treatments were well tolerated in men, albeit with a higher incidence of influenza-like illness and pyrexia events post-infusion with ZOL. Interpretation: Once-yearly ZOL preserves or increases BMD within 1 year to a greater extent than daily RIS in men receiving glucocorticoid therapy. |
| CC : | 002A16; 002B02L; 002B15A |
| FD : | Acide risédronique; Densité minérale osseuse; Bisphosphonates; Glucocorticoïde; Ostéoporose; Homme; Acide zolédronique; Morphologie; Antiostéoporotique; Antiostéoclastique |
| FG : | Pathologie du système ostéoarticulaire |
| ED : | Risedronic acid; Bone mineral density; Bisphosphonates; Glucocorticoid; Osteoporosis; Human; Zoledronic acid; Morphology; Antiosteoporotic; Antiosteoclastic agent |
| EG : | Diseases of the osteoarticular system |
| SD : | Acido risedrónico; Masa mineral ósea; Bisfosfonatos; Glucocorticoide; Osteoporosis; Hombre; Acido zoledrónico; Morfología; Antiosteoporótico; Antiosteoclástica |
| LO : | INIST-19041.354000509655900360 |
| ID : | 12-0182339 |
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Pascal:12-0182339Le document en format XML
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Sambrook</name><affiliation><inist:fA14 i1="01"><s1>University of Sydney</s1><s2>Sydney, NSW</s2><s3>AUS</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Roux, Christian" sort="Roux, Christian" uniqKey="Roux C" first="Christian" last="Roux">Christian Roux</name><affiliation><inist:fA14 i1="02"><s1>Paris-Descartes University</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Devogelaer, Jean Pierre" sort="Devogelaer, Jean Pierre" uniqKey="Devogelaer J" first="Jean-Pierre" last="Devogelaer">Jean-Pierre Devogelaer</name><affiliation><inist:fA14 i1="03"><s1>Université Catholique de Louvain at Brussels</s1><s2>Brussels</s2><s3>BEL</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Saag, Kenneth" sort="Saag, Kenneth" uniqKey="Saag K" first="Kenneth" last="Saag">Kenneth Saag</name><affiliation><inist:fA14 i1="04"><s1>University of Alabama at Birmingham</s1><s2>Birmingham, AL</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lau, Chak Sing" sort="Lau, Chak Sing" uniqKey="Lau C" first="Chak-Sing" last="Lau">Chak-Sing Lau</name><affiliation><inist:fA14 i1="05"><s1>University of Dundee</s1><s2>Dundee</s2><s3>GBR</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Reginster, Jean Yves" sort="Reginster, Jean Yves" uniqKey="Reginster J" first="Jean-Yves" last="Reginster">Jean-Yves Reginster</name><affiliation><inist:fA14 i1="06"><s1>University of Liège</s1><s2>Liège</s2><s3>BEL</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bucci Rechtweg, Christina" sort="Bucci Rechtweg, Christina" uniqKey="Bucci Rechtweg C" first="Christina" last="Bucci-Rechtweg">Christina Bucci-Rechtweg</name><affiliation><inist:fA14 i1="07"><s1>Novartis Pharmaceuticals Corporation</s1><s2>East Hanover, NJ</s2><s3>USA</s3><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Guoqin Su" sort="Guoqin Su" uniqKey="Guoqin Su" last="Guoqin Su">GUOQIN SU</name><affiliation><inist:fA14 i1="07"><s1>Novartis Pharmaceuticals Corporation</s1><s2>East Hanover, NJ</s2><s3>USA</s3><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Reid, David M" sort="Reid, David M" uniqKey="Reid D" first="David M." last="Reid">David M. Reid</name><affiliation><inist:fA14 i1="08"><s1>University of Aberdeen</s1><s2>Aberdeen</s2><s3>GBR</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">12-0182339</idno><date when="2012">2012</date><idno type="stanalyst">PASCAL 12-0182339 INIST</idno><idno type="RBID">Pascal:12-0182339</idno><idno type="wicri:Area/PascalFrancis/Corpus">001469</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate</title><author><name sortKey="Sambrook, Philip N" sort="Sambrook, Philip N" uniqKey="Sambrook P" first="Philip N." last="Sambrook">Philip N. Sambrook</name><affiliation><inist:fA14 i1="01"><s1>University of Sydney</s1><s2>Sydney, NSW</s2><s3>AUS</s3><sZ>1 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Roux, Christian" sort="Roux, Christian" uniqKey="Roux C" first="Christian" last="Roux">Christian Roux</name><affiliation><inist:fA14 i1="02"><s1>Paris-Descartes University</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Devogelaer, Jean Pierre" sort="Devogelaer, Jean Pierre" uniqKey="Devogelaer J" first="Jean-Pierre" last="Devogelaer">Jean-Pierre Devogelaer</name><affiliation><inist:fA14 i1="03"><s1>Université Catholique de Louvain at Brussels</s1><s2>Brussels</s2><s3>BEL</s3><sZ>3 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Saag, Kenneth" sort="Saag, Kenneth" uniqKey="Saag K" first="Kenneth" last="Saag">Kenneth Saag</name><affiliation><inist:fA14 i1="04"><s1>University of Alabama at Birmingham</s1><s2>Birmingham, AL</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Lau, Chak Sing" sort="Lau, Chak Sing" uniqKey="Lau C" first="Chak-Sing" last="Lau">Chak-Sing Lau</name><affiliation><inist:fA14 i1="05"><s1>University of Dundee</s1><s2>Dundee</s2><s3>GBR</s3><sZ>5 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Reginster, Jean Yves" sort="Reginster, Jean Yves" uniqKey="Reginster J" first="Jean-Yves" last="Reginster">Jean-Yves Reginster</name><affiliation><inist:fA14 i1="06"><s1>University of Liège</s1><s2>Liège</s2><s3>BEL</s3><sZ>6 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Bucci Rechtweg, Christina" sort="Bucci Rechtweg, Christina" uniqKey="Bucci Rechtweg C" first="Christina" last="Bucci-Rechtweg">Christina Bucci-Rechtweg</name><affiliation><inist:fA14 i1="07"><s1>Novartis Pharmaceuticals Corporation</s1><s2>East Hanover, NJ</s2><s3>USA</s3><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Guoqin Su" sort="Guoqin Su" uniqKey="Guoqin Su" last="Guoqin Su">GUOQIN SU</name><affiliation><inist:fA14 i1="07"><s1>Novartis Pharmaceuticals Corporation</s1><s2>East Hanover, NJ</s2><s3>USA</s3><sZ>7 aut.</sZ><sZ>8 aut.</sZ></inist:fA14></affiliation></author><author><name sortKey="Reid, David M" sort="Reid, David M" uniqKey="Reid D" first="David M." last="Reid">David M. Reid</name><affiliation><inist:fA14 i1="08"><s1>University of Aberdeen</s1><s2>Aberdeen</s2><s3>GBR</s3><sZ>9 aut.</sZ></inist:fA14></affiliation></author></analytic><series><title level="j" type="main">Bone : (New York, NY)</title><title level="j" type="abbreviated">Bone : (NY NY)</title><idno type="ISSN">8756-3282</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Bone : (New York, NY)</title><title level="j" type="abbreviated">Bone : (NY NY)</title><idno type="ISSN">8756-3282</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antiosteoclastic agent</term><term>Antiosteoporotic</term><term>Bisphosphonates</term><term>Bone mineral density</term><term>Glucocorticoid</term><term>Human</term><term>Morphology</term><term>Osteoporosis</term><term>Risedronic acid</term><term>Zoledronic acid</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Acide risédronique</term><term>Densité minérale osseuse</term><term>Bisphosphonates</term><term>Glucocorticoïde</term><term>Ostéoporose</term><term>Homme</term><term>Acide zolédronique</term><term>Morphologie</term><term>Antiostéoporotique</term><term>Antiostéoclastique</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background: We studied 265 men (mean age 56.4 years; range 18-83 years), among patients enrolled in two arms of a double-blind, 1-year study comparing the effects of zoledronic acid (ZOL) with risedronate (RIS) in patients either commencing (prednisolone 7.5 mg/day or equivalent) (prevention arm, n = 88) or continuing glucocorticoid therapy (treatment arm, n = 177). Methods: Patients received either a single ZOL 5 mg infusion or RIS 5 mg oral daily at randomization, along with calcium (1000 mg) and vitamin D (400-1200 IU). Primary endpoint: difference in percentage change from baseline in bone mineral density (BMD) at the lumbar spine (LS) at 12 months. Secondary endpoints: percentage changes in BMD at total hip (TH) and femoral neck (FN), relative changes in bone turnover markers (β-CTx and P1NP), and overall safety. Findings: In the treatment subpopulation, ZOL increased LS BMD by 4.7% vs. 3.3% for RIS and at TH the percentage changes were 1.8% vs. 0.2%, respectively. In the prevention subpopulation, bone loss was prevented by both treatments. At LS the percentage changes were 2.5% vs. - 0.2% for ZOL vs. RIS and at TH the percentage changes were 1.1% vs. -0.4%, respectively. ZOL significantly increased lumbar spine BMD more than RIS at Month 12 in both the prevention population (p=0.0024) and the treatment subpopulation (p = 0.0232) in men. In the treatment subpopulation, ZOL demonstrated a significantly greater reduction in serum β-CTx and P1NP relative to RIS at all time-points. In the prevention subpopulation, ZOL significantly reduced β-CTx at all time-points, and P1NP at Month 3 (p = 0.0297) only. Both treatments were well tolerated in men, albeit with a higher incidence of influenza-like illness and pyrexia events post-infusion with ZOL. Interpretation: Once-yearly ZOL preserves or increases BMD within 1 year to a greater extent than daily RIS in men receiving glucocorticoid therapy.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>8756-3282</s0></fA01><fA03 i2="1"><s0>Bone : (NY NY)</s0></fA03><fA05><s2>50</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate</s1></fA08><fA11 i1="01" i2="1"><s1>SAMBROOK (Philip N.)</s1></fA11><fA11 i1="02" i2="1"><s1>ROUX (Christian)</s1></fA11><fA11 i1="03" i2="1"><s1>DEVOGELAER (Jean-Pierre)</s1></fA11><fA11 i1="04" i2="1"><s1>SAAG (Kenneth)</s1></fA11><fA11 i1="05" i2="1"><s1>LAU (Chak-Sing)</s1></fA11><fA11 i1="06" i2="1"><s1>REGINSTER (Jean-Yves)</s1></fA11><fA11 i1="07" i2="1"><s1>BUCCI-RECHTWEG (Christina)</s1></fA11><fA11 i1="08" i2="1"><s1>GUOQIN SU</s1></fA11><fA11 i1="09" i2="1"><s1>REID (David M.)</s1></fA11><fA14 i1="01"><s1>University of Sydney</s1><s2>Sydney, NSW</s2><s3>AUS</s3><sZ>1 aut.</sZ></fA14><fA14 i1="02"><s1>Paris-Descartes University</s1><s2>Paris</s2><s3>FRA</s3><sZ>2 aut.</sZ></fA14><fA14 i1="03"><s1>Université Catholique de Louvain at Brussels</s1><s2>Brussels</s2><s3>BEL</s3><sZ>3 aut.</sZ></fA14><fA14 i1="04"><s1>University of Alabama at Birmingham</s1><s2>Birmingham, AL</s2><s3>USA</s3><sZ>4 aut.</sZ></fA14><fA14 i1="05"><s1>University of Dundee</s1><s2>Dundee</s2><s3>GBR</s3><sZ>5 aut.</sZ></fA14><fA14 i1="06"><s1>University of Liège</s1><s2>Liège</s2><s3>BEL</s3><sZ>6 aut.</sZ></fA14><fA14 i1="07"><s1>Novartis Pharmaceuticals Corporation</s1><s2>East Hanover, NJ</s2><s3>USA</s3><sZ>7 aut.</sZ><sZ>8 aut.</sZ></fA14><fA14 i1="08"><s1>University of Aberdeen</s1><s2>Aberdeen</s2><s3>GBR</s3><sZ>9 aut.</sZ></fA14><fA20><s1>289-295</s1></fA20><fA21><s1>2012</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>19041</s2><s5>354000509655900360</s5></fA43><fA44><s0>0000</s0><s1>© 2012 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>42 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>12-0182339</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Bone : (New York, NY)</s0></fA64><fA66 i1="01"><s0>NLD</s0></fA66><fC01 i1="01" l="ENG"><s0>Background: We studied 265 men (mean age 56.4 years; range 18-83 years), among patients enrolled in two arms of a double-blind, 1-year study comparing the effects of zoledronic acid (ZOL) with risedronate (RIS) in patients either commencing (prednisolone 7.5 mg/day or equivalent) (prevention arm, n = 88) or continuing glucocorticoid therapy (treatment arm, n = 177). Methods: Patients received either a single ZOL 5 mg infusion or RIS 5 mg oral daily at randomization, along with calcium (1000 mg) and vitamin D (400-1200 IU). Primary endpoint: difference in percentage change from baseline in bone mineral density (BMD) at the lumbar spine (LS) at 12 months. Secondary endpoints: percentage changes in BMD at total hip (TH) and femoral neck (FN), relative changes in bone turnover markers (β-CTx and P1NP), and overall safety. Findings: In the treatment subpopulation, ZOL increased LS BMD by 4.7% vs. 3.3% for RIS and at TH the percentage changes were 1.8% vs. 0.2%, respectively. In the prevention subpopulation, bone loss was prevented by both treatments. At LS the percentage changes were 2.5% vs. - 0.2% for ZOL vs. RIS and at TH the percentage changes were 1.1% vs. -0.4%, respectively. ZOL significantly increased lumbar spine BMD more than RIS at Month 12 in both the prevention population (p=0.0024) and the treatment subpopulation (p = 0.0232) in men. In the treatment subpopulation, ZOL demonstrated a significantly greater reduction in serum β-CTx and P1NP relative to RIS at all time-points. In the prevention subpopulation, ZOL significantly reduced β-CTx at all time-points, and P1NP at Month 3 (p = 0.0297) only. Both treatments were well tolerated in men, albeit with a higher incidence of influenza-like illness and pyrexia events post-infusion with ZOL. Interpretation: Once-yearly ZOL preserves or increases BMD within 1 year to a greater extent than daily RIS in men receiving glucocorticoid therapy.</s0></fC01><fC02 i1="01" i2="X"><s0>002A16</s0></fC02><fC02 i1="02" i2="X"><s0>002B02L</s0></fC02><fC02 i1="03" i2="X"><s0>002B15A</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Acide risédronique</s0><s2>NK</s2><s2>FR</s2><s5>04</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Risedronic acid</s0><s2>NK</s2><s2>FR</s2><s5>04</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Acido risedrónico</s0><s2>NK</s2><s2>FR</s2><s5>04</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Densité minérale osseuse</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Bone mineral density</s0><s5>05</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Masa mineral ósea</s0><s5>05</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Bisphosphonates</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Bisphosphonates</s0><s5>07</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Bisfosfonatos</s0><s5>07</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Glucocorticoïde</s0><s5>08</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Glucocorticoid</s0><s5>08</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Glucocorticoide</s0><s5>08</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Ostéoporose</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Osteoporosis</s0><s5>09</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Osteoporosis</s0><s5>09</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Homme</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Human</s0><s5>13</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Hombre</s0><s5>13</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Acide zolédronique</s0><s2>NK</s2><s2>FR</s2><s5>14</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Zoledronic acid</s0><s2>NK</s2><s2>FR</s2><s5>14</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Acido zoledrónico</s0><s2>NK</s2><s2>FR</s2><s5>14</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Morphologie</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Morphology</s0><s5>15</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Morfología</s0><s5>15</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Antiostéoporotique</s0><s5>30</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Antiosteoporotic</s0><s5>30</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Antiosteoporótico</s0><s5>30</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Antiostéoclastique</s0><s5>31</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Antiosteoclastic agent</s0><s5>31</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Antiosteoclástica</s0><s5>31</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Pathologie du système ostéoarticulaire</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Diseases of the osteoarticular system</s0><s5>37</s5></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Sistema osteoarticular patología</s0><s5>37</s5></fC07><fN21><s1>135</s1></fN21><fN44 i1="01"><s1>OTO</s1></fN44><fN82><s1>OTO</s1></fN82></pA></standard><server><NO>PASCAL 12-0182339 INIST</NO><ET>Bisphosphonates and glucocorticoid osteoporosis in men: results of a randomized controlled trial comparing zoledronic acid with risedronate</ET><AU>SAMBROOK (Philip N.); ROUX (Christian); DEVOGELAER (Jean-Pierre); SAAG (Kenneth); LAU (Chak-Sing); REGINSTER (Jean-Yves); BUCCI-RECHTWEG (Christina); GUOQIN SU; REID (David M.)</AU><AF>University of Sydney/Sydney, NSW/Australie (1 aut.); Paris-Descartes University/Paris/France (2 aut.); Université Catholique de Louvain at Brussels/Brussels/Belgique (3 aut.); University of Alabama at Birmingham/Birmingham, AL/Etats-Unis (4 aut.); University of Dundee/Dundee/Royaume-Uni (5 aut.); University of Liège/Liège/Belgique (6 aut.); Novartis Pharmaceuticals Corporation/East Hanover, NJ/Etats-Unis (7 aut., 8 aut.); University of Aberdeen/Aberdeen/Royaume-Uni (9 aut.)</AF><DT>Publication en série; Niveau analytique</DT><SO>Bone : (New York, NY); ISSN 8756-3282; Pays-Bas; Da. 2012; Vol. 50; No. 1; Pp. 289-295; Bibl. 42 ref.</SO><LA>Anglais</LA><EA>Background: We studied 265 men (mean age 56.4 years; range 18-83 years), among patients enrolled in two arms of a double-blind, 1-year study comparing the effects of zoledronic acid (ZOL) with risedronate (RIS) in patients either commencing (prednisolone 7.5 mg/day or equivalent) (prevention arm, n = 88) or continuing glucocorticoid therapy (treatment arm, n = 177). Methods: Patients received either a single ZOL 5 mg infusion or RIS 5 mg oral daily at randomization, along with calcium (1000 mg) and vitamin D (400-1200 IU). Primary endpoint: difference in percentage change from baseline in bone mineral density (BMD) at the lumbar spine (LS) at 12 months. Secondary endpoints: percentage changes in BMD at total hip (TH) and femoral neck (FN), relative changes in bone turnover markers (β-CTx and P1NP), and overall safety. Findings: In the treatment subpopulation, ZOL increased LS BMD by 4.7% vs. 3.3% for RIS and at TH the percentage changes were 1.8% vs. 0.2%, respectively. In the prevention subpopulation, bone loss was prevented by both treatments. At LS the percentage changes were 2.5% vs. - 0.2% for ZOL vs. RIS and at TH the percentage changes were 1.1% vs. -0.4%, respectively. ZOL significantly increased lumbar spine BMD more than RIS at Month 12 in both the prevention population (p=0.0024) and the treatment subpopulation (p = 0.0232) in men. In the treatment subpopulation, ZOL demonstrated a significantly greater reduction in serum β-CTx and P1NP relative to RIS at all time-points. In the prevention subpopulation, ZOL significantly reduced β-CTx at all time-points, and P1NP at Month 3 (p = 0.0297) only. Both treatments were well tolerated in men, albeit with a higher incidence of influenza-like illness and pyrexia events post-infusion with ZOL. Interpretation: Once-yearly ZOL preserves or increases BMD within 1 year to a greater extent than daily RIS in men receiving glucocorticoid therapy.</EA><CC>002A16; 002B02L; 002B15A</CC><FD>Acide risédronique; Densité minérale osseuse; Bisphosphonates; Glucocorticoïde; Ostéoporose; Homme; Acide zolédronique; Morphologie; Antiostéoporotique; Antiostéoclastique</FD><FG>Pathologie du système ostéoarticulaire</FG><ED>Risedronic acid; Bone mineral density; Bisphosphonates; Glucocorticoid; Osteoporosis; Human; Zoledronic acid; Morphology; Antiosteoporotic; Antiosteoclastic agent</ED><EG>Diseases of the osteoarticular system</EG><SD>Acido risedrónico; Masa mineral ósea; Bisfosfonatos; Glucocorticoide; Osteoporosis; Hombre; Acido zoledrónico; Morfología; Antiosteoporótico; Antiosteoclástica</SD><LO>INIST-19041.354000509655900360</LO><ID>12-0182339</ID></server></inist></record>Pour manipuler ce document sous Unix (Dilib)
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