Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients
Identifieur interne : 001991 ( Istex/Corpus ); précédent : 001990; suivant : 001992Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients
Auteurs : Yoshihiro Sato ; Yoshiaki Honda ; Jun Iwamoto ; Tomohiro Kanoko ; Kei SatohSource :
- Movement Disorders [ 0885-3185 ] ; 2005-12.
English descriptors
- KwdEn :
Abstract
To elucidate the influence of immobilization‐induced hypercalcemia on bone metabolism in Parkinson's disease (PD), we measured serum biochemical indexes and bone mineral density (BMD) in the second metacarpals of 142 elderly PD patients and 99 age‐matched healthy controls. Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 1,25‐dihydroxyvitamin D (1,25‐[OH]2D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D‐Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization‐induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25‐[OH]2D (mean, 88.7 pmol/L) and 25‐OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D‐Pyr concentration elevated. A negative correlation was observed between 1,25‐[OH]2D levels and serum calcium or UPDRS III (P < 0.0001). In disabled PD patients, immobilization‐induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25‐[OH]2D production. 25‐OHD insufficiency may also contribute to decreased 1,25‐[OH]2D. These abnormalities may be corrected by the suppression of bone resorption with bisphoshonate, and supplementations of calcium and vitamin D should be avoided in these patients. © 2005 Movement Disorder Society
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DOI: 10.1002/mds.20658
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Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 1,25‐dihydroxyvitamin D (1,25‐[OH]2D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D‐Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization‐induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25‐[OH]2D (mean, 88.7 pmol/L) and 25‐OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D‐Pyr concentration elevated. A negative correlation was observed between 1,25‐[OH]2D levels and serum calcium or UPDRS III (P < 0.0001). In disabled PD patients, immobilization‐induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25‐[OH]2D production. 25‐OHD insufficiency may also contribute to decreased 1,25‐[OH]2D. These abnormalities may be corrected by the suppression of bone resorption with bisphoshonate, and supplementations of calcium and vitamin D should be avoided in these patients. © 2005 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Yoshihiro Sato MD</name><affiliations><json:string>Department of Neurology, Mitate Hospital, Tagawa, Japan</json:string></affiliations></json:item><json:item><name>Yoshiaki Honda MD</name><affiliations><json:string>Department of Neurology, Mitate Hospital, Tagawa, Japan</json:string></affiliations></json:item><json:item><name>Jun Iwamoto MD</name><affiliations><json:string>Department of Sports Medicine, School of Medicine Keiko University, Tokyo, Japan</json:string></affiliations></json:item><json:item><name>Tomohiro Kanoko PhD</name><affiliations><json:string>Department of Rehabilitation Medicine, Hirosaki University School of Medicine, Hirosaki, Japan</json:string></affiliations></json:item><json:item><name>Kei Satoh MD</name><affiliations><json:string>Department of Vascular Biology, Hirosaki University School of Medicine, Hirosaki, Japan</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>bone mineral density</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>hypercalcemia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>immobilization</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>vitamin D</value></json:item></subject><language><json:string>eng</json:string></language><abstract>To elucidate the influence of immobilization‐induced hypercalcemia on bone metabolism in Parkinson's disease (PD), we measured serum biochemical indexes and bone mineral density (BMD) in the second metacarpals of 142 elderly PD patients and 99 age‐matched healthy controls. Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 1,25‐dihydroxyvitamin D (1,25‐[OH]2D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D‐Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization‐induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25‐[OH]2D (mean, 88.7 pmol/L) and 25‐OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D‐Pyr concentration elevated. A negative correlation was observed between 1,25‐[OH]2D levels and serum calcium or UPDRS III (P > 0.0001). In disabled PD patients, immobilization‐induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25‐[OH]2D production. 25‐OHD insufficiency may also contribute to decreased 1,25‐[OH]2D. 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Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 1,25‐dihydroxyvitamin D (1,25‐[OH]2D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D‐Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization‐induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25‐[OH]2D (mean, 88.7 pmol/L) and 25‐OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D‐Pyr concentration elevated. A negative correlation was observed between 1,25‐[OH]2D levels and serum calcium or UPDRS III (P < 0.0001). In disabled PD patients, immobilization‐induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25‐[OH]2D production. 25‐OHD insufficiency may also contribute to decreased 1,25‐[OH]2D. These abnormalities may be corrected by the suppression of bone resorption with bisphoshonate, and supplementations of calcium and vitamin D should be avoided in these patients. © 2005 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>bone mineral density</term></item><item><term>hypercalcemia</term></item><item><term>immobilization</term></item><item><term>vitamin D</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-02-18">Received</change><change when="2005-04-22">Registration</change><change when="2005-12">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9F165FED3C3A3AD3BCF95F1DDF752BD40DF5A498/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 1,25‐dihydroxyvitamin D (1,25‐[OH]<sub>2</sub>D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D‐Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization‐induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25‐[OH]<sub>2</sub>D (mean, 88.7 pmol/L) and 25‐OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D‐Pyr concentration elevated. A negative correlation was observed between 1,25‐[OH]<sub>2</sub>D levels and serum calcium or UPDRS III (<i>P</i> < 0.0001). In disabled PD patients, immobilization‐induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25‐[OH]<sub>2</sub>D production. 25‐OHD insufficiency may also contribute to decreased 1,25‐[OH]<sub>2</sub>D. These abnormalities may be corrected by the suppression of bone resorption with bisphoshonate, and supplementations of calcium and vitamin D should be avoided in these patients. © 2005 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Abnormal Bone and Calcium Metabolism</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients</title></titleInfo><name type="personal"><namePart type="given">Yoshihiro</namePart><namePart type="family">Sato</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan</affiliation><description>Correspondence: Department of Neurology, Mitate Hospital, Tagawa 826‐0041, Japan</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yoshiaki</namePart><namePart type="family">Honda</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jun</namePart><namePart type="family">Iwamoto</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Sports Medicine, School of Medicine Keiko University, Tokyo, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tomohiro</namePart><namePart type="family">Kanoko</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Department of Rehabilitation Medicine, Hirosaki University School of Medicine, Hirosaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kei</namePart><namePart type="family">Satoh</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Vascular Biology, Hirosaki University School of Medicine, Hirosaki, Japan</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-12</dateIssued><dateCaptured encoding="w3cdtf">2005-02-18</dateCaptured><dateValid encoding="w3cdtf">2005-04-22</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">3</extent><extent unit="references">38</extent><extent unit="words">3811</extent></physicalDescription><abstract lang="en">To elucidate the influence of immobilization‐induced hypercalcemia on bone metabolism in Parkinson's disease (PD), we measured serum biochemical indexes and bone mineral density (BMD) in the second metacarpals of 142 elderly PD patients and 99 age‐matched healthy controls. Serum concentrations of 25‐hydroxyvitamin D (25‐OHD), 1,25‐dihydroxyvitamin D (1,25‐[OH]2D), ionized calcium, intact parathyroid hormone (PTH), and intact bone Gla protein (BGP) were measured. Urinary deoxypyridinoline (D‐Pyr) was also measured. Increased serum calcium levels (mean, 1.27 mmol/L) were observed in PD patients, and the levels correlated negatively with the Unified Parkinson's Disease Rating Scale III (UPDRS III), indicating the presence of immobilization‐induced bone resorption with resultant hypercalcemia. Decreased serum concentrations of 1,25‐[OH]2D (mean, 88.7 pmol/L) and 25‐OHD (mean, 29.7 nmol/L) were noted. Serum PTH was decreased (mean, 25.2 ng/L). Serum BGP was decreased while urinary D‐Pyr concentration elevated. A negative correlation was observed between 1,25‐[OH]2D levels and serum calcium or UPDRS III (P < 0.0001). In disabled PD patients, immobilization‐induced hypercalcemia may inhibit secretion of PTH, which in turn suppresses 1,25‐[OH]2D production. 25‐OHD insufficiency may also contribute to decreased 1,25‐[OH]2D. These abnormalities may be corrected by the suppression of bone resorption with bisphoshonate, and supplementations of calcium and vitamin D should be avoided in these patients. © 2005 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>bone mineral density</topic><topic>hypercalcemia</topic><topic>immobilization</topic><topic>vitamin D</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>12</number></detail><extent unit="pages"><start>1598</start><end>1603</end><total>6</total></extent></part></relatedItem><identifier type="istex">9F165FED3C3A3AD3BCF95F1DDF752BD40DF5A498</identifier><identifier type="DOI">10.1002/mds.20658</identifier><identifier type="ArticleID">MDS20658</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2005 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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