Homocysteine-lowering therapy or antioxidant therapy for bone loss in Parkinson's disease.
Identifieur interne : 002904 ( Ncbi/Merge ); précédent : 002903; suivant : 002905Homocysteine-lowering therapy or antioxidant therapy for bone loss in Parkinson's disease.
Auteurs : Seung Hun Lee [Corée du Sud] ; Mi Jung Kim ; Beom-Jun Kim ; Sung Reul Kim ; Sail Chun ; Jin Sook Ryu ; Ghi Su Kim ; Myoung Chong Lee ; Jung-Min Koh ; Sun Ju ChungSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2010.
English descriptors
- KwdEn :
- Absorptiometry, Photon (methods), Aged, Analysis of Variance, Anthropometry (methods), Antioxidants (therapeutic use), Bone Demineralization, Pathologic (drug therapy), Bone Demineralization, Pathologic (etiology), Bone Demineralization, Pathologic (pathology), Bone Density (drug effects), Collagen Type I (metabolism), Female, Follow-Up Studies, Homocysteine (metabolism), Humans, Male, Middle Aged, Parkinson Disease (complications), Peptides (metabolism), Thioctic Acid (therapeutic use).
- MESH :
- chemical , metabolism : Collagen Type I, Homocysteine, Peptides.
- chemical , therapeutic use : Antioxidants, Thioctic Acid.
- complications : Parkinson Disease.
- drug effects : Bone Density.
- drug therapy : Bone Demineralization, Pathologic.
- etiology : Bone Demineralization, Pathologic.
- methods : Absorptiometry, Photon, Anthropometry.
- pathology : Bone Demineralization, Pathologic.
- Aged, Analysis of Variance, Female, Follow-Up Studies, Humans, Male, Middle Aged.
Abstract
We investigated whether homocysteine (Hcy)- lowering therapy or an antioxidant prevented bone loss in Parkinson's disease (PD) patients taking levodopa. Forty-two PD patients with low bone mineral density (BMD) taking levodopa were randomly assigned to Hcy-lowering therapy (5 mg folate and 1500 microg vitamin B(12) daily), alpha-lipoic acid (alpha-LA) therapy (1200 mg daily), or control groups. Primary outcomes were BMD changes from baseline to 12 months. Secondary outcomes were changes in Hcy level, and C-telopeptide (CTX) levels at 12 months. Forty-one patients completed the study. Hcy-lowering therapy resulted in significantly greater BMD changes at the lumbar spine (4.4%), total femur (2.8%), and femur shaft (2.8%) than control (P = 0.005-0.023). BMD changes in the alpha-LA therapy group were similar to those of the control group, but changes at the trochanter (4.6%) were significantly greater in the alpha-LA therapy group than in the control group after adjustment for body mass index changes. Hcy concentrations decreased to 35.2% +/- 13.4% in the Hcy-lowering therapy group, but increased in other groups. Serum CTX levels at 12 months tended to be lower in the Hcy-lowering group (0.442 +/- 0.024 ng/mL) than control group (0.628 +/- 0.039 ng/mL) (P = 0.159). This small trial suggests that Hcy-lowering therapy may prevent bone loss in PD patients taking levodopa.
DOI: 10.1002/mds.22866
PubMed: 19938151
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Kim</name></author><author><name sortKey="Kim, Sung Reul" sort="Kim, Sung Reul" uniqKey="Kim S" first="Sung Reul" last="Kim">Sung Reul Kim</name></author><author><name sortKey="Chun, Sail" sort="Chun, Sail" uniqKey="Chun S" first="Sail" last="Chun">Sail Chun</name></author><author><name sortKey="Ryu, Jin Sook" sort="Ryu, Jin Sook" uniqKey="Ryu J" first="Jin Sook" last="Ryu">Jin Sook Ryu</name></author><author><name sortKey="Kim, Ghi Su" sort="Kim, Ghi Su" uniqKey="Kim G" first="Ghi Su" last="Kim">Ghi Su Kim</name></author><author><name sortKey="Lee, Myoung Chong" sort="Lee, Myoung Chong" uniqKey="Lee M" first="Myoung Chong" last="Lee">Myoung Chong Lee</name></author><author><name sortKey="Koh, Jung Min" sort="Koh, Jung Min" uniqKey="Koh J" first="Jung-Min" last="Koh">Jung-Min Koh</name></author><author><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name></author></titleStmt><publicationStmt><idno 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Ulsan College of Medicine, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation></author><author><name sortKey="Kim, Mi Jung" sort="Kim, Mi Jung" uniqKey="Kim M" first="Mi Jung" last="Kim">Mi Jung Kim</name></author><author><name sortKey="Kim, Beom Jun" sort="Kim, Beom Jun" uniqKey="Kim B" first="Beom-Jun" last="Kim">Beom-Jun Kim</name></author><author><name sortKey="Kim, Sung Reul" sort="Kim, Sung Reul" uniqKey="Kim S" first="Sung Reul" last="Kim">Sung Reul Kim</name></author><author><name sortKey="Chun, Sail" sort="Chun, Sail" uniqKey="Chun S" first="Sail" last="Chun">Sail Chun</name></author><author><name sortKey="Ryu, Jin Sook" sort="Ryu, Jin Sook" uniqKey="Ryu J" first="Jin Sook" last="Ryu">Jin Sook Ryu</name></author><author><name sortKey="Kim, Ghi Su" sort="Kim, Ghi Su" uniqKey="Kim G" first="Ghi Su" last="Kim">Ghi Su Kim</name></author><author><name sortKey="Lee, Myoung Chong" sort="Lee, Myoung Chong" uniqKey="Lee M" first="Myoung Chong" last="Lee">Myoung Chong Lee</name></author><author><name sortKey="Koh, Jung Min" sort="Koh, Jung Min" uniqKey="Koh J" first="Jung-Min" last="Koh">Jung-Min Koh</name></author><author><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Absorptiometry, Photon (methods)</term><term>Aged</term><term>Analysis of Variance</term><term>Anthropometry (methods)</term><term>Antioxidants (therapeutic use)</term><term>Bone Demineralization, Pathologic (drug therapy)</term><term>Bone Demineralization, Pathologic (etiology)</term><term>Bone Demineralization, Pathologic (pathology)</term><term>Bone Density (drug effects)</term><term>Collagen Type I (metabolism)</term><term>Female</term><term>Follow-Up Studies</term><term>Homocysteine (metabolism)</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Peptides (metabolism)</term><term>Thioctic Acid (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Collagen Type I</term><term>Homocysteine</term><term>Peptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antioxidants</term><term>Thioctic Acid</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Bone Density</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Bone Demineralization, Pathologic</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Bone Demineralization, Pathologic</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Absorptiometry, Photon</term><term>Anthropometry</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Bone Demineralization, Pathologic</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Analysis of Variance</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We investigated whether homocysteine (Hcy)- lowering therapy or an antioxidant prevented bone loss in Parkinson's disease (PD) patients taking levodopa. Forty-two PD patients with low bone mineral density (BMD) taking levodopa were randomly assigned to Hcy-lowering therapy (5 mg folate and 1500 microg vitamin B(12) daily), alpha-lipoic acid (alpha-LA) therapy (1200 mg daily), or control groups. Primary outcomes were BMD changes from baseline to 12 months. Secondary outcomes were changes in Hcy level, and C-telopeptide (CTX) levels at 12 months. Forty-one patients completed the study. Hcy-lowering therapy resulted in significantly greater BMD changes at the lumbar spine (4.4%), total femur (2.8%), and femur shaft (2.8%) than control (P = 0.005-0.023). BMD changes in the alpha-LA therapy group were similar to those of the control group, but changes at the trochanter (4.6%) were significantly greater in the alpha-LA therapy group than in the control group after adjustment for body mass index changes. Hcy concentrations decreased to 35.2% +/- 13.4% in the Hcy-lowering therapy group, but increased in other groups. Serum CTX levels at 12 months tended to be lower in the Hcy-lowering group (0.442 +/- 0.024 ng/mL) than control group (0.628 +/- 0.039 ng/mL) (P = 0.159). This small trial suggests that Hcy-lowering therapy may prevent bone loss in PD patients taking levodopa.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">19938151</PMID><DateCreated><Year>2010</Year><Month>03</Month><Day>03</Day></DateCreated><DateCompleted><Year>2010</Year><Month>06</Month><Day>02</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>25</Volume><Issue>3</Issue><PubDate><Year>2010</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Homocysteine-lowering therapy or antioxidant therapy for bone loss in Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>332-40</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22866</ELocationID><Abstract><AbstractText>We investigated whether homocysteine (Hcy)- lowering therapy or an antioxidant prevented bone loss in Parkinson's disease (PD) patients taking levodopa. Forty-two PD patients with low bone mineral density (BMD) taking levodopa were randomly assigned to Hcy-lowering therapy (5 mg folate and 1500 microg vitamin B(12) daily), alpha-lipoic acid (alpha-LA) therapy (1200 mg daily), or control groups. Primary outcomes were BMD changes from baseline to 12 months. Secondary outcomes were changes in Hcy level, and C-telopeptide (CTX) levels at 12 months. Forty-one patients completed the study. Hcy-lowering therapy resulted in significantly greater BMD changes at the lumbar spine (4.4%), total femur (2.8%), and femur shaft (2.8%) than control (P = 0.005-0.023). BMD changes in the alpha-LA therapy group were similar to those of the control group, but changes at the trochanter (4.6%) were significantly greater in the alpha-LA therapy group than in the control group after adjustment for body mass index changes. Hcy concentrations decreased to 35.2% +/- 13.4% in the Hcy-lowering therapy group, but increased in other groups. Serum CTX levels at 12 months tended to be lower in the Hcy-lowering group (0.442 +/- 0.024 ng/mL) than control group (0.628 +/- 0.039 ng/mL) (P = 0.159). This small trial suggests that Hcy-lowering therapy may prevent bone loss in PD patients taking levodopa.</AbstractText><CopyrightInformation>(c) 2009 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Seung Hun</ForeName><Initials>SH</Initials><AffiliationInfo><Affiliation>Division of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Mi Jung</ForeName><Initials>MJ</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Beom-Jun</ForeName><Initials>BJ</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Sung Reul</ForeName><Initials>SR</Initials></Author><Author ValidYN="Y"><LastName>Chun</LastName><ForeName>Sail</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Ryu</LastName><ForeName>Jin Sook</ForeName><Initials>JS</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Ghi Su</ForeName><Initials>GS</Initials></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Myoung Chong</ForeName><Initials>MC</Initials></Author><Author ValidYN="Y"><LastName>Koh</LastName><ForeName>Jung-Min</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Chung</LastName><ForeName>Sun Ju</ForeName><Initials>SJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000975">Antioxidants</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D024042">Collagen Type I</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C052929">collagen type I trimeric cross-linked peptide</NameOfSubstance></Chemical><Chemical><RegistryNumber>0LVT1QZ0BA</RegistryNumber><NameOfSubstance UI="D006710">Homocysteine</NameOfSubstance></Chemical><Chemical><RegistryNumber>73Y7P0K73Y</RegistryNumber><NameOfSubstance UI="D008063">Thioctic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015502">Absorptiometry, Photon</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><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="D000886">Anthropometry</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000379">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000975">Antioxidants</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018488">Bone Demineralization, Pathologic</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000209">etiology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015519">Bone Density</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D024042">Collagen Type I</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005500">Follow-Up Studies</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006710">Homocysteine</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</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="Q000150">complications</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010455">Peptides</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008063">Thioctic Acid</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2009</Year><Month>11</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2009</Year><Month>11</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2010</Year><Month>6</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.22866</ArticleId><ArticleId IdType="pubmed">19938151</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Corée du Sud</li></country><settlement><li>Séoul</li></settlement></list><tree><noCountry><name sortKey="Chun, Sail" sort="Chun, Sail" uniqKey="Chun S" first="Sail" last="Chun">Sail Chun</name><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name><name sortKey="Kim, Beom Jun" sort="Kim, Beom Jun" uniqKey="Kim B" first="Beom-Jun" last="Kim">Beom-Jun Kim</name><name sortKey="Kim, Ghi Su" sort="Kim, Ghi Su" uniqKey="Kim G" first="Ghi Su" last="Kim">Ghi Su Kim</name><name sortKey="Kim, Mi Jung" sort="Kim, Mi Jung" uniqKey="Kim M" first="Mi Jung" last="Kim">Mi Jung Kim</name><name sortKey="Kim, Sung Reul" sort="Kim, Sung Reul" uniqKey="Kim S" first="Sung Reul" last="Kim">Sung Reul Kim</name><name sortKey="Koh, Jung Min" sort="Koh, Jung Min" uniqKey="Koh J" first="Jung-Min" last="Koh">Jung-Min Koh</name><name sortKey="Lee, Myoung Chong" sort="Lee, Myoung Chong" uniqKey="Lee M" first="Myoung Chong" last="Lee">Myoung Chong Lee</name><name sortKey="Ryu, Jin Sook" sort="Ryu, Jin Sook" uniqKey="Ryu J" first="Jin Sook" last="Ryu">Jin Sook Ryu</name></noCountry><country name="Corée du Sud"><noRegion><name sortKey="Lee, Seung Hun" sort="Lee, Seung Hun" uniqKey="Lee S" first="Seung Hun" last="Lee">Seung Hun Lee</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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