Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients.
Identifieur interne : 003267 ( PubMed/Curation ); précédent : 003266; suivant : 003268Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients.
Auteurs : Paolo Lamberti [Italie] ; Stefano Zoccolella ; Giovanni Iliceto ; Elio Armenise ; Angela Fraddosio ; Michele De Mari ; Paolo LivreaSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2005.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Case-Control Studies, Catechols (pharmacology), Catechols (therapeutic use), Chromatography, High Pressure Liquid (methods), Drug Therapy, Combination, Female, Folic Acid (blood), Homocysteine (blood), Humans, Levodopa (pharmacology), Levodopa (therapeutic use), Linear Models, Male, Middle Aged, Nitriles, Parkinson Disease (blood), Parkinson Disease (drug therapy), Vitamin B 12 (blood).
- MESH :
- chemical , blood : Folic Acid, Homocysteine, Vitamin B 12.
- chemical , pharmacology : Antiparkinson Agents, Catechols, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Catechols, Levodopa.
- blood : Parkinson Disease.
- drug therapy : Parkinson Disease.
- methods : Chromatography, High Pressure Liquid.
- Aged, Case-Control Studies, Drug Therapy, Combination, Female, Humans, Linear Models, Male, Middle Aged, Nitriles.
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.
DOI: 10.1002/mds.20261
PubMed: 15390046
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pubmed:15390046Le document en format XML
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<affiliation wicri:level="1"><nlm:affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy. lamberti@neurol.uniba.it</nlm:affiliation>
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<wicri:regionArea>Department of Neurological Sciences, University of Bari, Bari</wicri:regionArea>
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<author><name sortKey="Iliceto, Giovanni" sort="Iliceto, Giovanni" uniqKey="Iliceto G" first="Giovanni" last="Iliceto">Giovanni Iliceto</name>
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<author><name sortKey="Armenise, Elio" sort="Armenise, Elio" uniqKey="Armenise E" first="Elio" last="Armenise">Elio Armenise</name>
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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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<Abstract><AbstractText>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.</AbstractText>
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