Homocysteine‐lowering therapy or antioxidant therapy for bone loss in Parkinson's disease
Identifieur interne : 001C51 ( Main/Exploration ); précédent : 001C50; suivant : 001C52Homocysteine‐lowering therapy or antioxidant therapy for bone loss in Parkinson's disease
Auteurs : Seung Hun Lee [Corée du Sud] ; Mi Jung Kim [Corée du Sud] ; Beom-Jun Kim [Corée du Sud] ; Sung Reul Kim [Corée du Sud] ; Sail Chun [Corée du Sud] ; Jin Sook Ryu [Corée du Sud] ; Ghi Su Kim [Corée du Sud] ; Myoung Chong Lee [Corée du Sud] ; Jung-Min Koh [Corée du Sud] ; Sun Ju Chung [Corée du Sud]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-02-15.
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), Parkinson's disease, Peptides (metabolism), Thioctic Acid (therapeutic use), folate, homocysteine, osteoporosis, vitamin B12.
- 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 μg vitamin B12 daily), α‐lipoic acid (α‐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 α–LA therapy group were similar to those of the control group, but changes at the trochanter (4.6%) were significantly greater in the α–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. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22866
Affiliations:
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sortKey="Ryu, Jin Sook" sort="Ryu, Jin Sook" uniqKey="Ryu J" first="Jin Sook" last="Ryu">Jin Sook Ryu</name><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Nuclear Medicine, 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, Ghi Su" sort="Kim, Ghi Su" uniqKey="Kim G" first="Ghi Su" last="Kim">Ghi Su Kim</name><affiliation wicri:level="3"><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="Lee, Myoung Chong" sort="Lee, Myoung Chong" uniqKey="Lee M" first="Myoung Chong" last="Lee">Myoung Chong Lee</name><affiliation wicri:level="3"><country 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Neurology, Asan Medical Center, University of Ulsan College of Medicine, 388‐1 Poongnap2‐Dong, Songpa‐Gu, Seoul 138‐736</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation></author><author><name sortKey="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr" wicri:curation="lc">Corée du Sud</country><wicri:regionArea>Jung‐Min Koh, Division of Endocrinology and Metabolism, Asan Medical Center, University of Ulsan College of Medicine, 388‐1 Poongnap2‐Dong, Songpa‐Gu, Seoul 138‐736, Republic of Korea===Sun Ju Chung, Department of Neurology, Asan Medical Center, University 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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010-02-15">2010-02-15</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="332">332</biblScope><biblScope unit="page" to="340">340</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">C94E2240071BC7B3006C42D566F6CC5761602DFA</idno><idno type="DOI">10.1002/mds.22866</idno><idno type="ArticleID">MDS22866</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></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>Parkinson's disease</term><term>Peptides (metabolism)</term><term>Thioctic Acid (therapeutic use)</term><term>folate</term><term>homocysteine</term><term>osteoporosis</term><term>vitamin B12</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><langUsage><language ident="en">en</language></langUsage></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 μg vitamin B12 daily), α‐lipoic acid (α‐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 α–LA therapy group were similar to those of the control group, but changes at the trochanter (4.6%) were significantly greater in the α–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. © 2009 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Corée du Sud</li></country><settlement><li>Séoul</li></settlement></list><tree><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><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="Chung, Sun Ju" sort="Chung, Sun Ju" uniqKey="Chung S" first="Sun Ju" last="Chung">Sun Ju Chung</name><name sortKey="Kim, Beom Un" sort="Kim, Beom Un" 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 In" sort="Koh, Jung In" uniqKey="Koh J" first="Jung-Min" last="Koh">Jung-Min Koh</name><name sortKey="Koh, Jung In" sort="Koh, Jung In" 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></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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