The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelter's syndrome: the influence of vitamin D deficiency and hormonal status
The aim of this study was to evaluate the effects of a 2-year treatment with intravenous ibandronate (2 mg every 3 months) and calcium (1000 mg daily) on bone mineral density (BMD) and bone markers in 14 patients with Klinefelter's syndrome who served as their own controls. During the follow-up...
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| Veröffentlicht in: | Bone (New York, N.Y.) N.Y.), 2003-10, Vol.33 (4), p.589-596 |
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| description | The aim of this study was to evaluate the effects of a 2-year treatment with intravenous ibandronate (2 mg every 3 months) and calcium (1000 mg daily) on bone mineral density (BMD) and bone markers in 14 patients with Klinefelter's syndrome who served as their own controls. During the follow-up of 5.9 years before the treatment was started, the mean rates of bone loss per year were 1.3, 0.9, and 0.6% in the lumbar spine, femoral neck, and total body, respectively. The rate of bone loss from the spine was significantly inversely related to both serum estradiol and testosterone. At the onset of treatment, the average age of the patients was 55.2 years (48–64 years), and T score, mean ± SD, at the lumbar spine was −2.6 ± 1.0. After 6 months, the mean serum CTX and PINP decreased by 39 and 55% below the pretreatment concentrations, respectively (P < 0.05). After 12 months of treatment, the patients gained mean ± SD, 7.8 ± 2.3% of BMD in the lumbar spine, 3.8 ± 4.0% in the femoral neck, and 4.7 ± 2.2% in the total body (P < 0.05). During the second year of treatment, all patients also received 700 IU of vitamin D daily. After 24 months of treatment, the patients gained 10.1 ± 4.3% of BMD in the lumbar spine, 6.7 ± 5.5% in the femoral neck, and 5.5 ± 2.5% in the total body. The increase in BMD in the second year of ibandronate treatment was not significant. The rate of gain of BMD in the femoral neck was positively related to serum concentrations of testosterone and inversely related to 25-hydroxyvitamin D (P < 0.005). After the discontinuation of treatment, serum CTX and PINP increased to the pretreatment levels, and the lumbar spine and femur neck BMD decreased (P < 0.05). In conclusion, ibandronate was effective in increasing BMD at all sites, but the effects were adversely influenced by vitamin D insufficiency or deficiency. The overall changes in biochemical markers of bone remodeling were consistent with the antiresorptive effect of the drug. |
| doi_str_mv | 10.1016/S8756-3282(03)00205-9 |
| format | Article |
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During the follow-up of 5.9 years before the treatment was started, the mean rates of bone loss per year were 1.3, 0.9, and 0.6% in the lumbar spine, femoral neck, and total body, respectively. The rate of bone loss from the spine was significantly inversely related to both serum estradiol and testosterone. At the onset of treatment, the average age of the patients was 55.2 years (48–64 years), and T score, mean ± SD, at the lumbar spine was −2.6 ± 1.0. After 6 months, the mean serum CTX and PINP decreased by 39 and 55% below the pretreatment concentrations, respectively (P < 0.05). After 12 months of treatment, the patients gained mean ± SD, 7.8 ± 2.3% of BMD in the lumbar spine, 3.8 ± 4.0% in the femoral neck, and 4.7 ± 2.2% in the total body (P < 0.05). During the second year of treatment, all patients also received 700 IU of vitamin D daily. After 24 months of treatment, the patients gained 10.1 ± 4.3% of BMD in the lumbar spine, 6.7 ± 5.5% in the femoral neck, and 5.5 ± 2.5% in the total body. The increase in BMD in the second year of ibandronate treatment was not significant. The rate of gain of BMD in the femoral neck was positively related to serum concentrations of testosterone and inversely related to 25-hydroxyvitamin D (P < 0.005). After the discontinuation of treatment, serum CTX and PINP increased to the pretreatment levels, and the lumbar spine and femur neck BMD decreased (P < 0.05). In conclusion, ibandronate was effective in increasing BMD at all sites, but the effects were adversely influenced by vitamin D insufficiency or deficiency. The overall changes in biochemical markers of bone remodeling were consistent with the antiresorptive effect of the drug.</description><identifier>ISSN: 8756-3282</identifier><identifier>EISSN: 1873-2763</identifier><identifier>DOI: 10.1016/S8756-3282(03)00205-9</identifier><identifier>PMID: 14555263</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adult ; Aged ; Biochemical markers ; Biological and medical sciences ; Bone Density - drug effects ; Bone mineral density ; Bone Remodeling - drug effects ; Bones, joints and connective tissue. Antiinflammatory agents ; Collagen - urine ; Collagen Type I ; Diphosphonates - administration & dosage ; Diphosphonates - therapeutic use ; Estradiol - blood ; Humans ; Hypogonadism ; Ibandronic Acid ; Injections, Intravenous ; Klinefelter Syndrome - complications ; Klinefelter Syndrome - drug therapy ; Klinefelter Syndrome - metabolism ; Male ; Medical sciences ; Middle Aged ; Osteoporosis ; Peptide Fragments - blood ; Peptides - urine ; Pharmacology. Drug treatments ; Procollagen - blood ; Testosterone ; Testosterone - blood ; Time Factors ; Vitamin D Deficiency - complications</subject><ispartof>Bone (New York, N.Y.), 2003-10, Vol.33 (4), p.589-596</ispartof><rights>2003 Elsevier Inc.</rights><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c422t-7507c66513bfb3aebaeef2a3b3c32e3ea2262c5d6cf5a492517d9816d4deef283</citedby><cites>FETCH-LOGICAL-c422t-7507c66513bfb3aebaeef2a3b3c32e3ea2262c5d6cf5a492517d9816d4deef283</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S8756-3282(03)00205-9$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15201056$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14555263$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Stepan, Jan J</creatorcontrib><creatorcontrib>Burckhardt, Peter</creatorcontrib><creatorcontrib>Hána, Václav</creatorcontrib><title>The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelter's syndrome: the influence of vitamin D deficiency and hormonal status</title><title>Bone (New York, N.Y.)</title><addtitle>Bone</addtitle><description>The aim of this study was to evaluate the effects of a 2-year treatment with intravenous ibandronate (2 mg every 3 months) and calcium (1000 mg daily) on bone mineral density (BMD) and bone markers in 14 patients with Klinefelter's syndrome who served as their own controls. During the follow-up of 5.9 years before the treatment was started, the mean rates of bone loss per year were 1.3, 0.9, and 0.6% in the lumbar spine, femoral neck, and total body, respectively. The rate of bone loss from the spine was significantly inversely related to both serum estradiol and testosterone. At the onset of treatment, the average age of the patients was 55.2 years (48–64 years), and T score, mean ± SD, at the lumbar spine was −2.6 ± 1.0. After 6 months, the mean serum CTX and PINP decreased by 39 and 55% below the pretreatment concentrations, respectively (P < 0.05). After 12 months of treatment, the patients gained mean ± SD, 7.8 ± 2.3% of BMD in the lumbar spine, 3.8 ± 4.0% in the femoral neck, and 4.7 ± 2.2% in the total body (P < 0.05). During the second year of treatment, all patients also received 700 IU of vitamin D daily. After 24 months of treatment, the patients gained 10.1 ± 4.3% of BMD in the lumbar spine, 6.7 ± 5.5% in the femoral neck, and 5.5 ± 2.5% in the total body. The increase in BMD in the second year of ibandronate treatment was not significant. The rate of gain of BMD in the femoral neck was positively related to serum concentrations of testosterone and inversely related to 25-hydroxyvitamin D (P < 0.005). After the discontinuation of treatment, serum CTX and PINP increased to the pretreatment levels, and the lumbar spine and femur neck BMD decreased (P < 0.05). In conclusion, ibandronate was effective in increasing BMD at all sites, but the effects were adversely influenced by vitamin D insufficiency or deficiency. The overall changes in biochemical markers of bone remodeling were consistent with the antiresorptive effect of the drug.</description><subject>Adult</subject><subject>Aged</subject><subject>Biochemical markers</subject><subject>Biological and medical sciences</subject><subject>Bone Density - drug effects</subject><subject>Bone mineral density</subject><subject>Bone Remodeling - drug effects</subject><subject>Bones, joints and connective tissue. Antiinflammatory agents</subject><subject>Collagen - urine</subject><subject>Collagen Type I</subject><subject>Diphosphonates - administration & dosage</subject><subject>Diphosphonates - therapeutic use</subject><subject>Estradiol - blood</subject><subject>Humans</subject><subject>Hypogonadism</subject><subject>Ibandronic Acid</subject><subject>Injections, Intravenous</subject><subject>Klinefelter Syndrome - complications</subject><subject>Klinefelter Syndrome - drug therapy</subject><subject>Klinefelter Syndrome - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Osteoporosis</subject><subject>Peptide Fragments - blood</subject><subject>Peptides - urine</subject><subject>Pharmacology. Drug treatments</subject><subject>Procollagen - blood</subject><subject>Testosterone</subject><subject>Testosterone - blood</subject><subject>Time Factors</subject><subject>Vitamin D Deficiency - complications</subject><issn>8756-3282</issn><issn>1873-2763</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFksuOFCEUhitG47Sjj6Bh421RyqWALjfGjNc4iQvHNaHgYGOqYAaoTvq5fEGpro6znBWE853_Pzk_TfOU4DcEE_H251Zy0TK6pa8we40xxbzt7zUbspWspVKw-83mP3LWPMr5D8aY9ZI8bM5Ixzmngm2av1c7QOAcmJJRdKjsEkA7xVB2yIeS9B5CnDPygw42xaALoBjQEAOgyQdIekQWQvblgCqxFhJM0cLow--qgb7XCzgYC6SXGeXDojPBu2oFtezGGYKBxXvvi66a6GNVdN74-r6K7mKqE1WnXHSZ8-PmgdNjhien87z59fnT1cXX9vLHl28XHy5b01FaWsmxNEJwwgY3MA2DBnBUs4EZRoGBplRQw60wjuuup5xI22-JsJ1dwC07b16sutcp3syQi5p8NjCOOkDdiZJcik5geSdIekopZosiX0GTYs4JnLpOftLpoAhWS6zqGKtaMlOYqWOsqq99z04G8zCBve065ViB5ydAZ6NHl3QwPt9ynGKCuajc-5WDure9h6Tycc9gfapfQNno7xjlHybzw1w</recordid><startdate>20031001</startdate><enddate>20031001</enddate><creator>Stepan, Jan J</creator><creator>Burckhardt, Peter</creator><creator>Hána, Václav</creator><general>Elsevier Inc</general><general>Elsevier Science</general><scope>IQODW</scope><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>7QP</scope><scope>7X8</scope></search><sort><creationdate>20031001</creationdate><title>The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelter's syndrome: the influence of vitamin D deficiency and hormonal status</title><author>Stepan, Jan J ; Burckhardt, Peter ; Hána, Václav</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c422t-7507c66513bfb3aebaeef2a3b3c32e3ea2262c5d6cf5a492517d9816d4deef283</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biochemical markers</topic><topic>Biological and medical sciences</topic><topic>Bone Density - drug effects</topic><topic>Bone mineral density</topic><topic>Bone Remodeling - drug effects</topic><topic>Bones, joints and connective tissue. Antiinflammatory agents</topic><topic>Collagen - urine</topic><topic>Collagen Type I</topic><topic>Diphosphonates - administration & dosage</topic><topic>Diphosphonates - therapeutic use</topic><topic>Estradiol - blood</topic><topic>Humans</topic><topic>Hypogonadism</topic><topic>Ibandronic Acid</topic><topic>Injections, Intravenous</topic><topic>Klinefelter Syndrome - complications</topic><topic>Klinefelter Syndrome - drug therapy</topic><topic>Klinefelter Syndrome - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Osteoporosis</topic><topic>Peptide Fragments - blood</topic><topic>Peptides - urine</topic><topic>Pharmacology. Drug treatments</topic><topic>Procollagen - blood</topic><topic>Testosterone</topic><topic>Testosterone - blood</topic><topic>Time Factors</topic><topic>Vitamin D Deficiency - complications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stepan, Jan J</creatorcontrib><creatorcontrib>Burckhardt, Peter</creatorcontrib><creatorcontrib>Hána, Václav</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Bone (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stepan, Jan J</au><au>Burckhardt, Peter</au><au>Hána, Václav</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelter's syndrome: the influence of vitamin D deficiency and hormonal status</atitle><jtitle>Bone (New York, N.Y.)</jtitle><addtitle>Bone</addtitle><date>2003-10-01</date><risdate>2003</risdate><volume>33</volume><issue>4</issue><spage>589</spage><epage>596</epage><pages>589-596</pages><issn>8756-3282</issn><eissn>1873-2763</eissn><abstract>The aim of this study was to evaluate the effects of a 2-year treatment with intravenous ibandronate (2 mg every 3 months) and calcium (1000 mg daily) on bone mineral density (BMD) and bone markers in 14 patients with Klinefelter's syndrome who served as their own controls. During the follow-up of 5.9 years before the treatment was started, the mean rates of bone loss per year were 1.3, 0.9, and 0.6% in the lumbar spine, femoral neck, and total body, respectively. The rate of bone loss from the spine was significantly inversely related to both serum estradiol and testosterone. At the onset of treatment, the average age of the patients was 55.2 years (48–64 years), and T score, mean ± SD, at the lumbar spine was −2.6 ± 1.0. After 6 months, the mean serum CTX and PINP decreased by 39 and 55% below the pretreatment concentrations, respectively (P < 0.05). After 12 months of treatment, the patients gained mean ± SD, 7.8 ± 2.3% of BMD in the lumbar spine, 3.8 ± 4.0% in the femoral neck, and 4.7 ± 2.2% in the total body (P < 0.05). During the second year of treatment, all patients also received 700 IU of vitamin D daily. After 24 months of treatment, the patients gained 10.1 ± 4.3% of BMD in the lumbar spine, 6.7 ± 5.5% in the femoral neck, and 5.5 ± 2.5% in the total body. The increase in BMD in the second year of ibandronate treatment was not significant. The rate of gain of BMD in the femoral neck was positively related to serum concentrations of testosterone and inversely related to 25-hydroxyvitamin D (P < 0.005). After the discontinuation of treatment, serum CTX and PINP increased to the pretreatment levels, and the lumbar spine and femur neck BMD decreased (P < 0.05). In conclusion, ibandronate was effective in increasing BMD at all sites, but the effects were adversely influenced by vitamin D insufficiency or deficiency. The overall changes in biochemical markers of bone remodeling were consistent with the antiresorptive effect of the drug.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>14555263</pmid><doi>10.1016/S8756-3282(03)00205-9</doi><tpages>8</tpages></addata></record> |
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| subjects | Adult Aged Biochemical markers Biological and medical sciences Bone Density - drug effects Bone mineral density Bone Remodeling - drug effects Bones, joints and connective tissue. Antiinflammatory agents Collagen - urine Collagen Type I Diphosphonates - administration & dosage Diphosphonates - therapeutic use Estradiol - blood Humans Hypogonadism Ibandronic Acid Injections, Intravenous Klinefelter Syndrome - complications Klinefelter Syndrome - drug therapy Klinefelter Syndrome - metabolism Male Medical sciences Middle Aged Osteoporosis Peptide Fragments - blood Peptides - urine Pharmacology. Drug treatments Procollagen - blood Testosterone Testosterone - blood Time Factors Vitamin D Deficiency - complications |
| title | The effects of three-month intravenous ibandronate on bone mineral density and bone remodeling in Klinefelter's syndrome: the influence of vitamin D deficiency and hormonal status |
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