Homocysteine-lowering therapy or antioxidant therapy for bone loss in Parkinson's disease.
Identifieur interne : 002904 ( Ncbi/Curation ); 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 type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="doi">10.1002/mds.22866</idno><idno type="RBID">pubmed:19938151</idno><idno type="pmid">19938151</idno><idno type="wicri:Area/PubMed/Corpus">001A79</idno><idno type="wicri:Area/PubMed/Curation">001A79</idno><idno type="wicri:Area/PubMed/Checkpoint">001847</idno><idno type="wicri:Area/Ncbi/Merge">002904</idno><idno type="wicri:Area/Ncbi/Curation">002904</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Homocysteine-lowering therapy or antioxidant therapy for bone loss in Parkinson's disease.</title><author><name sortKey="Lee, Seung Hun" sort="Lee, Seung Hun" uniqKey="Lee S" first="Seung Hun" last="Lee">Seung Hun Lee</name><affiliation wicri:level="3"><nlm:affiliation>Division of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.</nlm:affiliation><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Division of Endocrinology and Metabolism, Asan Medical Center, University of 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></record>Pour manipuler ce document sous Unix (Dilib)
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