Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients.
Identifieur interne : 002F05 ( PubMed/Curation ); précédent : 002F04; suivant : 002F06Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients.
Auteurs : Yoshihiro Sato [Japon] ; Yoshiaki Honda ; Jun Iwamoto ; Tomohiro Kanoko ; Kei SatohSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Aged, Analysis of Variance, Bone Density (physiology), Bone Diseases, Metabolic (blood), Bone Diseases, Metabolic (etiology), Calcium (metabolism), Case-Control Studies, Female, Humans, Immobilization, Linear Models, Male, Middle Aged, Parkinson Disease (blood), Parkinson Disease (complications), Retrospective Studies, Vitamin D (analogs & derivatives), Vitamin D (blood).
- MESH :
- chemical , analogs & derivatives : Vitamin D.
- chemical , blood : Vitamin D.
- chemical , metabolism : Calcium.
- blood : Bone Diseases, Metabolic, Parkinson Disease.
- complications : Parkinson Disease.
- etiology : Bone Diseases, Metabolic.
- physiology : Bone Density.
- Aged, Analysis of Variance, Case-Control Studies, Female, Humans, Immobilization, Linear Models, Male, Middle Aged, Retrospective Studies.
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](2)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](2)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](2)D 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](2)D production. 25-OHD insufficiency may also contribute to decreased 1,25-[OH](2)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.
DOI: 10.1002/mds.20658
PubMed: 16114020
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients.</title><author><name sortKey="Sato, Yoshihiro" sort="Sato, Yoshihiro" uniqKey="Sato Y" first="Yoshihiro" last="Sato">Yoshihiro Sato</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan. y-sato@ktarn.or.jp</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Mitate Hospital, Tagawa</wicri:regionArea></affiliation></author><author><name sortKey="Honda, Yoshiaki" sort="Honda, Yoshiaki" uniqKey="Honda Y" first="Yoshiaki" last="Honda">Yoshiaki Honda</name></author><author><name sortKey="Iwamoto, Jun" sort="Iwamoto, Jun" uniqKey="Iwamoto J" first="Jun" last="Iwamoto">Jun Iwamoto</name></author><author><name sortKey="Kanoko, Tomohiro" sort="Kanoko, Tomohiro" uniqKey="Kanoko T" first="Tomohiro" last="Kanoko">Tomohiro Kanoko</name></author><author><name sortKey="Satoh, Kei" sort="Satoh, Kei" uniqKey="Satoh K" first="Kei" last="Satoh">Kei Satoh</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="doi">10.1002/mds.20658</idno><idno type="RBID">pubmed:16114020</idno><idno type="pmid">16114020</idno><idno type="wicri:Area/PubMed/Corpus">002F05</idno><idno type="wicri:Area/PubMed/Curation">002F05</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients.</title><author><name sortKey="Sato, Yoshihiro" sort="Sato, Yoshihiro" uniqKey="Sato Y" first="Yoshihiro" last="Sato">Yoshihiro Sato</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan. y-sato@ktarn.or.jp</nlm:affiliation><country xml:lang="fr">Japon</country><wicri:regionArea>Department of Neurology, Mitate Hospital, Tagawa</wicri:regionArea></affiliation></author><author><name sortKey="Honda, Yoshiaki" sort="Honda, Yoshiaki" uniqKey="Honda Y" first="Yoshiaki" last="Honda">Yoshiaki Honda</name></author><author><name sortKey="Iwamoto, Jun" sort="Iwamoto, Jun" uniqKey="Iwamoto J" first="Jun" last="Iwamoto">Jun Iwamoto</name></author><author><name sortKey="Kanoko, Tomohiro" sort="Kanoko, Tomohiro" uniqKey="Kanoko T" first="Tomohiro" last="Kanoko">Tomohiro Kanoko</name></author><author><name sortKey="Satoh, Kei" sort="Satoh, Kei" uniqKey="Satoh K" first="Kei" last="Satoh">Kei Satoh</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Bone Density (physiology)</term><term>Bone Diseases, Metabolic (blood)</term><term>Bone Diseases, Metabolic (etiology)</term><term>Calcium (metabolism)</term><term>Case-Control Studies</term><term>Female</term><term>Humans</term><term>Immobilization</term><term>Linear Models</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (blood)</term><term>Parkinson Disease (complications)</term><term>Retrospective Studies</term><term>Vitamin D (analogs & derivatives)</term><term>Vitamin D (blood)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Vitamin D</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Vitamin D</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Calcium</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Bone Diseases, Metabolic</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Bone Diseases, Metabolic</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Bone Density</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Case-Control Studies</term><term>Female</term><term>Humans</term><term>Immobilization</term><term>Linear Models</term><term>Male</term><term>Middle Aged</term><term>Retrospective Studies</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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](2)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](2)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](2)D 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](2)D production. 25-OHD insufficiency may also contribute to decreased 1,25-[OH](2)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.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">16114020</PMID><DateCreated><Year>2005</Year><Month>11</Month><Day>07</Day></DateCreated><DateCompleted><Year>2006</Year><Month>03</Month><Day>21</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>20</Volume><Issue>12</Issue><PubDate><Year>2005</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Abnormal bone and calcium metabolism in immobilized Parkinson's disease patients.</ArticleTitle><Pagination><MedlinePgn>1598-603</MedlinePgn></Pagination><Abstract><AbstractText>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](2)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](2)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](2)D 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](2)D production. 25-OHD insufficiency may also contribute to decreased 1,25-[OH](2)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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sato</LastName><ForeName>Yoshihiro</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Neurology, Mitate Hospital, Tagawa, Japan. y-sato@ktarn.or.jp</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Honda</LastName><ForeName>Yoshiaki</ForeName><Initials>Y</Initials></Author><Author ValidYN="Y"><LastName>Iwamoto</LastName><ForeName>Jun</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Kanoko</LastName><ForeName>Tomohiro</ForeName><Initials>T</Initials></Author><Author ValidYN="Y"><LastName>Satoh</LastName><ForeName>Kei</ForeName><Initials>K</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>1406-16-2</RegistryNumber><NameOfSubstance UI="D014807">Vitamin D</NameOfSubstance></Chemical><Chemical><RegistryNumber>64719-49-9</RegistryNumber><NameOfSubstance UI="C104450">25-hydroxyvitamin D</NameOfSubstance></Chemical><Chemical><RegistryNumber>66772-14-3</RegistryNumber><NameOfSubstance UI="C097949">1,25-dihydroxyvitamin D</NameOfSubstance></Chemical><Chemical><RegistryNumber>SY7Q814VUP</RegistryNumber><NameOfSubstance UI="D002118">Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000704">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015519">Bone Density</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000502">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001851">Bone Diseases, Metabolic</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002118">Calcium</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016022">Case-Control Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D007103">Immobilization</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016014">Linear Models</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012189">Retrospective Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014807">Vitamin D</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000031">analogs & derivatives</QualifierName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2005</Year><Month>8</Month><Day>23</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2006</Year><Month>3</Month><Day>22</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2005</Year><Month>8</Month><Day>23</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.20658</ArticleId><ArticleId IdType="pubmed">16114020</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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