Effects of levodopa and COMT inhibitors on plasma Homocysteine in Parkinson's disease patients
Identifieur interne : 001F44 ( PascalFrancis/Corpus ); précédent : 001F43; suivant : 001F45Effects 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 LivreaSource :
- Movement disorders [ 0885-3185 ] ; 2005.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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)
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Format Inist (serveur)
NO : | PASCAL 05-0173268 INIST |
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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:05-0173268Le document en format XML
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<front><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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<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>
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