Movement Disorders (revue)

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Effects of levodopa and COMT inhibitors on plasma Homocysteine in Parkinson's disease patients

Identifieur interne : 001F44 ( PascalFrancis/Corpus ); précédent : 001F43; suivant : 001F45

Effects of levodopa and COMT inhibitors on plasma Homocysteine in Parkinson's disease patients

Auteurs : Paolo Lamberti ; Stefano Zoccolella ; Giovanni Iliceto ; Elio Armenise ; Angela Fraddosio ; Michele De Mari ; Paolo Livrea

Source :

RBID : Pascal:05-0173268

Descripteurs français

English descriptors

Abstract

Homocysteine (Hcy) is a risk factor for vascular diseases, cognitive impairment, and dementia. Elevated plasma concentrations of Hcy have been found recently in Parkinson's disease (PD) patients treated with levodopa, suggesting that levodopa is a cause of hyperhomocysteinemia (HHcy). The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. COMT inhibitors (COMT-I) are used currently in the treatment of PD; however, no study has assessed the effects of COMT-I administration on Hcy concentrations in PD patients. We compared plasma levels of Hcy, B12, and folate in 26 PD patients treated with levodopa, 20 PD patients treated with levodopa + COMT-I, and 32 controls. No significant differences were found in vitamin B12 levels, whereas folate concentrations were significantly lower in the levodopa-treated group. Plasma Hcy was increased significantly in the two groups of PD patients and was significantly lower in the group treated with levodopa + COMT-I. Statistical analysis showed that the difference in mean Hcy levels observed among PD patients was related to the addition of COMT-I, rather than to folate concentrations. We conclude that levodopa treatment increases plasma Hcy and the addition of COMT-I effectively reduces HHcy.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A01 01  1    @0 0885-3185
A03   1    @0 Mov. disord.
A05       @2 20
A06       @2 1
A08 01  1  ENG  @1 Effects of levodopa and COMT inhibitors on plasma Homocysteine in Parkinson's disease patients
A11 01  1    @1 LAMBERTI (Paolo)
A11 02  1    @1 ZOCCOLELLA (Stefano)
A11 03  1    @1 ILICETO (Giovanni)
A11 04  1    @1 ARMENISE (Elio)
A11 05  1    @1 FRADDOSIO (Angela)
A11 06  1    @1 DE MARI (Michele)
A11 07  1    @1 LIVREA (Paolo)
A14 01      @1 Department of Neurological Sciences, University of Bari @2 Bari @3 ITA @Z 1 aut. @Z 2 aut. @Z 3 aut. @Z 5 aut. @Z 6 aut. @Z 7 aut.
A14 02      @1 Department of Internal Medicine and Public Health-Hygiene Section, University of Bari @2 Bari @3 ITA @Z 4 aut.
A20       @1 69-72
A21       @1 2005
A23 01      @0 ENG
A43 01      @1 INIST @2 20953 @5 354000125001470100
A44       @0 0000 @1 © 2005 INIST-CNRS. All rights reserved.
A45       @0 16 ref.
A47 01  1    @0 05-0173268
A60       @1 P @3 CC
A61       @0 A
A64 01  1    @0 Movement disorders
A66 01      @0 USA
C01 01    ENG  @0 Homocysteine (Hcy) is a risk factor for vascular diseases, cognitive impairment, and dementia. Elevated plasma concentrations of Hcy have been found recently in Parkinson's disease (PD) patients treated with levodopa, suggesting that levodopa is a cause of hyperhomocysteinemia (HHcy). The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. COMT inhibitors (COMT-I) are used currently in the treatment of PD; however, no study has assessed the effects of COMT-I administration on Hcy concentrations in PD patients. We compared plasma levels of Hcy, B12, and folate in 26 PD patients treated with levodopa, 20 PD patients treated with levodopa + COMT-I, and 32 controls. No significant differences were found in vitamin B12 levels, whereas folate concentrations were significantly lower in the levodopa-treated group. Plasma Hcy was increased significantly in the two groups of PD patients and was significantly lower in the group treated with levodopa + COMT-I. Statistical analysis showed that the difference in mean Hcy levels observed among PD patients was related to the addition of COMT-I, rather than to folate concentrations. We conclude that levodopa treatment increases plasma Hcy and the addition of COMT-I effectively reduces HHcy.
C02 01  X    @0 002B17
C02 02  X    @0 002B17G
C02 03  X    @0 002B02U01
C03 01  X  FRE  @0 Système nerveux pathologie @5 01
C03 01  X  ENG  @0 Nervous system diseases @5 01
C03 01  X  SPA  @0 Sistema nervioso patología @5 01
C03 02  X  FRE  @0 Lévodopa @2 NK @2 FR @5 02
C03 02  X  ENG  @0 Levodopa @2 NK @2 FR @5 02
C03 02  X  SPA  @0 Levodopa @2 NK @2 FR @5 02
C03 03  X  FRE  @0 Homocystéine @2 NK @2 FR @5 03
C03 03  X  ENG  @0 Homocystein @2 NK @2 FR @5 03
C03 03  X  SPA  @0 Homocisteína @2 NK @2 FR @5 03
C03 04  X  FRE  @0 Parkinson maladie @5 04
C03 04  X  ENG  @0 Parkinson disease @5 04
C03 04  X  SPA  @0 Parkinson enfermedad @5 04
C03 05  X  FRE  @0 Homme @5 05
C03 05  X  ENG  @0 Human @5 05
C03 05  X  SPA  @0 Hombre @5 05
C07 01  X  FRE  @0 Antiparkinsonien @5 37
C07 01  X  ENG  @0 Antiparkinson agent @5 37
C07 01  X  SPA  @0 Antiparkinsoniano @5 37
C07 02  X  FRE  @0 Encéphale pathologie @5 38
C07 02  X  ENG  @0 Cerebral disorder @5 38
C07 02  X  SPA  @0 Encéfalo patología @5 38
C07 03  X  FRE  @0 Extrapyramidal syndrome @5 39
C07 03  X  ENG  @0 Extrapyramidal syndrome @5 39
C07 03  X  SPA  @0 Extrapiramidal síndrome @5 39
C07 04  X  FRE  @0 Maladie dégénérative @5 40
C07 04  X  ENG  @0 Degenerative disease @5 40
C07 04  X  SPA  @0 Enfermedad degenerativa @5 40
C07 05  X  FRE  @0 Système nerveux central pathologie @5 41
C07 05  X  ENG  @0 Central nervous system disease @5 41
C07 05  X  SPA  @0 Sistema nervosio central patología @5 41
N21       @1 115
N44 01      @1 OTO
N82       @1 OTO

Format Inist (serveur)

NO : PASCAL 05-0173268 INIST
ET : Effects of levodopa and COMT inhibitors on plasma Homocysteine in Parkinson's disease patients
AU : LAMBERTI (Paolo); ZOCCOLELLA (Stefano); ILICETO (Giovanni); ARMENISE (Elio); FRADDOSIO (Angela); DE MARI (Michele); LIVREA (Paolo)
AF : Department of Neurological Sciences, University of Bari/Bari/Italie (1 aut., 2 aut., 3 aut., 5 aut., 6 aut., 7 aut.); Department of Internal Medicine and Public Health-Hygiene Section, University of Bari/Bari/Italie (4 aut.)
DT : Publication en série; Courte communication, note brève; Niveau analytique
SO : Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 1; Pp. 69-72; Bibl. 16 ref.
LA : Anglais
EA : Homocysteine (Hcy) is a risk factor for vascular diseases, cognitive impairment, and dementia. Elevated plasma concentrations of Hcy have been found recently in Parkinson's disease (PD) patients treated with levodopa, suggesting that levodopa is a cause of hyperhomocysteinemia (HHcy). The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. COMT inhibitors (COMT-I) are used currently in the treatment of PD; however, no study has assessed the effects of COMT-I administration on Hcy concentrations in PD patients. We compared plasma levels of Hcy, B12, and folate in 26 PD patients treated with levodopa, 20 PD patients treated with levodopa + COMT-I, and 32 controls. No significant differences were found in vitamin B12 levels, whereas folate concentrations were significantly lower in the levodopa-treated group. Plasma Hcy was increased significantly in the two groups of PD patients and was significantly lower in the group treated with levodopa + COMT-I. Statistical analysis showed that the difference in mean Hcy levels observed among PD patients was related to the addition of COMT-I, rather than to folate concentrations. We conclude that levodopa treatment increases plasma Hcy and the addition of COMT-I effectively reduces HHcy.
CC : 002B17; 002B17G; 002B02U01
FD : Système nerveux pathologie; Lévodopa; Homocystéine; Parkinson maladie; Homme
FG : Antiparkinsonien; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie
ED : Nervous system diseases; Levodopa; Homocystein; Parkinson disease; Human
EG : Antiparkinson agent; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease
SD : Sistema nervioso patología; Levodopa; Homocisteína; Parkinson enfermedad; Hombre
LO : INIST-20953.354000125001470100
ID : 05-0173268

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Pascal:05-0173268

Le document en format XML

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<div type="abstract" xml:lang="en">Homocysteine (Hcy) is a risk factor for vascular diseases, cognitive impairment, and dementia. Elevated plasma concentrations of Hcy have been found recently in Parkinson's disease (PD) patients treated with levodopa, suggesting that levodopa is a cause of hyperhomocysteinemia (HHcy). The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. COMT inhibitors (COMT-I) are used currently in the treatment of PD; however, no study has assessed the effects of COMT-I administration on Hcy concentrations in PD patients. We compared plasma levels of Hcy, B12, and folate in 26 PD patients treated with levodopa, 20 PD patients treated with levodopa + COMT-I, and 32 controls. No significant differences were found in vitamin B12 levels, whereas folate concentrations were significantly lower in the levodopa-treated group. Plasma Hcy was increased significantly in the two groups of PD patients and was significantly lower in the group treated with levodopa + COMT-I. Statistical analysis showed that the difference in mean Hcy levels observed among PD patients was related to the addition of COMT-I, rather than to folate concentrations. We conclude that levodopa treatment increases plasma Hcy and the addition of COMT-I effectively reduces HHcy.</div>
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<s0>Homocysteine (Hcy) is a risk factor for vascular diseases, cognitive impairment, and dementia. Elevated plasma concentrations of Hcy have been found recently in Parkinson's disease (PD) patients treated with levodopa, suggesting that levodopa is a cause of hyperhomocysteinemia (HHcy). The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. COMT inhibitors (COMT-I) are used currently in the treatment of PD; however, no study has assessed the effects of COMT-I administration on Hcy concentrations in PD patients. We compared plasma levels of Hcy, B12, and folate in 26 PD patients treated with levodopa, 20 PD patients treated with levodopa + COMT-I, and 32 controls. No significant differences were found in vitamin B12 levels, whereas folate concentrations were significantly lower in the levodopa-treated group. Plasma Hcy was increased significantly in the two groups of PD patients and was significantly lower in the group treated with levodopa + COMT-I. Statistical analysis showed that the difference in mean Hcy levels observed among PD patients was related to the addition of COMT-I, rather than to folate concentrations. We conclude that levodopa treatment increases plasma Hcy and the addition of COMT-I effectively reduces HHcy.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X">
<s0>002B02U01</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Lévodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Homocystéine</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Homocystein</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Homocisteína</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Parkinson maladie</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Parkinson disease</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Parkinson enfermedad</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Homme</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Human</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Hombre</s0>
<s5>05</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Antiparkinsonien</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Antiparkinson agent</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Antiparkinsoniano</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>41</s5>
</fC07>
<fN21>
<s1>115</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
<server>
<NO>PASCAL 05-0173268 INIST</NO>
<ET>Effects of levodopa and COMT inhibitors on plasma Homocysteine in Parkinson's disease patients</ET>
<AU>LAMBERTI (Paolo); ZOCCOLELLA (Stefano); ILICETO (Giovanni); ARMENISE (Elio); FRADDOSIO (Angela); DE MARI (Michele); LIVREA (Paolo)</AU>
<AF>Department of Neurological Sciences, University of Bari/Bari/Italie (1 aut., 2 aut., 3 aut., 5 aut., 6 aut., 7 aut.); Department of Internal Medicine and Public Health-Hygiene Section, University of Bari/Bari/Italie (4 aut.)</AF>
<DT>Publication en série; Courte communication, note brève; Niveau analytique</DT>
<SO>Movement disorders; ISSN 0885-3185; Etats-Unis; Da. 2005; Vol. 20; No. 1; Pp. 69-72; Bibl. 16 ref.</SO>
<LA>Anglais</LA>
<EA>Homocysteine (Hcy) is a risk factor for vascular diseases, cognitive impairment, and dementia. Elevated plasma concentrations of Hcy have been found recently in Parkinson's disease (PD) patients treated with levodopa, suggesting that levodopa is a cause of hyperhomocysteinemia (HHcy). The mechanism underlying HHcy in PD is the O-methylation of levodopa catalyzed by catechol-O-methyltransferase (COMT) that produces S-adenosylhomocysteine, which is hydrolyzed rapidly to Hcy. COMT inhibitors (COMT-I) are used currently in the treatment of PD; however, no study has assessed the effects of COMT-I administration on Hcy concentrations in PD patients. We compared plasma levels of Hcy, B12, and folate in 26 PD patients treated with levodopa, 20 PD patients treated with levodopa + COMT-I, and 32 controls. No significant differences were found in vitamin B12 levels, whereas folate concentrations were significantly lower in the levodopa-treated group. Plasma Hcy was increased significantly in the two groups of PD patients and was significantly lower in the group treated with levodopa + COMT-I. Statistical analysis showed that the difference in mean Hcy levels observed among PD patients was related to the addition of COMT-I, rather than to folate concentrations. We conclude that levodopa treatment increases plasma Hcy and the addition of COMT-I effectively reduces HHcy.</EA>
<CC>002B17; 002B17G; 002B02U01</CC>
<FD>Système nerveux pathologie; Lévodopa; Homocystéine; Parkinson maladie; Homme</FD>
<FG>Antiparkinsonien; Encéphale pathologie; Extrapyramidal syndrome; Maladie dégénérative; Système nerveux central pathologie</FG>
<ED>Nervous system diseases; Levodopa; Homocystein; Parkinson disease; Human</ED>
<EG>Antiparkinson agent; Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Sistema nervioso patología; Levodopa; Homocisteína; Parkinson enfermedad; Hombre</SD>
<LO>INIST-20953.354000125001470100</LO>
<ID>05-0173268</ID>
</server>
</inist>
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