Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients.
Identifieur interne : 003151 ( PubMed/Checkpoint ); précédent : 003150; suivant : 003152Effects 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
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients.</title><author><name sortKey="Lamberti, Paolo" sort="Lamberti, Paolo" uniqKey="Lamberti P" first="Paolo" last="Lamberti">Paolo Lamberti</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy. lamberti@neurol.uniba.it</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Neurological Sciences, University of Bari, Bari</wicri:regionArea><wicri:noRegion>Bari</wicri:noRegion></affiliation></author><author><name sortKey="Zoccolella, Stefano" sort="Zoccolella, Stefano" uniqKey="Zoccolella S" first="Stefano" last="Zoccolella">Stefano Zoccolella</name></author><author><name sortKey="Iliceto, Giovanni" sort="Iliceto, Giovanni" uniqKey="Iliceto G" first="Giovanni" last="Iliceto">Giovanni Iliceto</name></author><author><name sortKey="Armenise, Elio" sort="Armenise, Elio" uniqKey="Armenise E" first="Elio" last="Armenise">Elio Armenise</name></author><author><name sortKey="Fraddosio, Angela" sort="Fraddosio, Angela" uniqKey="Fraddosio A" first="Angela" last="Fraddosio">Angela Fraddosio</name></author><author><name sortKey="De Mari, Michele" sort="De Mari, Michele" uniqKey="De Mari M" first="Michele" last="De Mari">Michele De Mari</name></author><author><name sortKey="Livrea, Paolo" sort="Livrea, Paolo" uniqKey="Livrea P" first="Paolo" last="Livrea">Paolo Livrea</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2005">2005</date><idno type="RBID">pubmed:15390046</idno><idno type="pmid">15390046</idno><idno type="doi">10.1002/mds.20261</idno><idno type="wicri:Area/PubMed/Corpus">003267</idno><idno type="wicri:Area/PubMed/Curation">003267</idno><idno type="wicri:Area/PubMed/Checkpoint">003151</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients.</title><author><name sortKey="Lamberti, Paolo" sort="Lamberti, Paolo" uniqKey="Lamberti P" first="Paolo" last="Lamberti">Paolo Lamberti</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy. lamberti@neurol.uniba.it</nlm:affiliation><country xml:lang="fr">Italie</country><wicri:regionArea>Department of Neurological Sciences, University of Bari, Bari</wicri:regionArea><wicri:noRegion>Bari</wicri:noRegion></affiliation></author><author><name sortKey="Zoccolella, Stefano" sort="Zoccolella, Stefano" uniqKey="Zoccolella S" first="Stefano" last="Zoccolella">Stefano Zoccolella</name></author><author><name sortKey="Iliceto, Giovanni" sort="Iliceto, Giovanni" uniqKey="Iliceto G" first="Giovanni" last="Iliceto">Giovanni Iliceto</name></author><author><name sortKey="Armenise, Elio" sort="Armenise, Elio" uniqKey="Armenise E" first="Elio" last="Armenise">Elio Armenise</name></author><author><name sortKey="Fraddosio, Angela" sort="Fraddosio, Angela" uniqKey="Fraddosio A" first="Angela" last="Fraddosio">Angela Fraddosio</name></author><author><name sortKey="De Mari, Michele" sort="De Mari, Michele" uniqKey="De Mari M" first="Michele" last="De Mari">Michele De Mari</name></author><author><name sortKey="Livrea, Paolo" sort="Livrea, Paolo" uniqKey="Livrea P" first="Paolo" last="Livrea">Paolo Livrea</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="2005" type="published">2005</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Case-Control Studies</term><term>Catechols (pharmacology)</term><term>Catechols (therapeutic use)</term><term>Chromatography, High Pressure Liquid (methods)</term><term>Drug Therapy, Combination</term><term>Female</term><term>Folic Acid (blood)</term><term>Homocysteine (blood)</term><term>Humans</term><term>Levodopa (pharmacology)</term><term>Levodopa (therapeutic use)</term><term>Linear Models</term><term>Male</term><term>Middle Aged</term><term>Nitriles</term><term>Parkinson Disease (blood)</term><term>Parkinson Disease (drug therapy)</term><term>Vitamin B 12 (blood)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Folic Acid</term><term>Homocysteine</term><term>Vitamin B 12</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Catechols</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Catechols</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Chromatography, High Pressure Liquid</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Case-Control Studies</term><term>Drug Therapy, Combination</term><term>Female</term><term>Humans</term><term>Linear Models</term><term>Male</term><term>Middle Aged</term><term>Nitriles</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">15390046</PMID><DateCreated><Year>2005</Year><Month>01</Month><Day>24</Day></DateCreated><DateCompleted><Year>2005</Year><Month>05</Month><Day>09</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>20</Volume><Issue>1</Issue><PubDate><Year>2005</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients.</ArticleTitle><Pagination><MedlinePgn>69-72</MedlinePgn></Pagination><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><CopyrightInformation>(c) 2004 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lamberti</LastName><ForeName>Paolo</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy. lamberti@neurol.uniba.it</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zoccolella</LastName><ForeName>Stefano</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Iliceto</LastName><ForeName>Giovanni</ForeName><Initials>G</Initials></Author><Author ValidYN="Y"><LastName>Armenise</LastName><ForeName>Elio</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Fraddosio</LastName><ForeName>Angela</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>de Mari</LastName><ForeName>Michele</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Livrea</LastName><ForeName>Paolo</ForeName><Initials>P</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016430">Clinical Trial</PublicationType><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002396">Catechols</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009570">Nitriles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0LVT1QZ0BA</RegistryNumber><NameOfSubstance UI="D006710">Homocysteine</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>4975G9NM6T</RegistryNumber><NameOfSubstance UI="C071192">entacapone</NameOfSubstance></Chemical><Chemical><RegistryNumber>935E97BOY8</RegistryNumber><NameOfSubstance UI="D005492">Folic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>P6YC3EG204</RegistryNumber><NameOfSubstance UI="D014805">Vitamin B 12</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="Y" 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MajorTopicYN="N" UI="Q000097">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006710">Homocysteine</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000097">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016014">Linear Models</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009570">Nitriles</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014805">Vitamin B 12</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>9</Month><Day>25</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2005</Year><Month>5</Month><Day>10</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>9</Month><Day>25</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15390046</ArticleId><ArticleId IdType="doi">10.1002/mds.20261</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Italie</li></country></list><tree><noCountry><name sortKey="Armenise, Elio" sort="Armenise, Elio" uniqKey="Armenise E" first="Elio" last="Armenise">Elio Armenise</name><name sortKey="De Mari, Michele" sort="De Mari, Michele" uniqKey="De Mari M" first="Michele" last="De Mari">Michele De Mari</name><name sortKey="Fraddosio, Angela" sort="Fraddosio, Angela" uniqKey="Fraddosio A" first="Angela" last="Fraddosio">Angela Fraddosio</name><name sortKey="Iliceto, Giovanni" sort="Iliceto, Giovanni" uniqKey="Iliceto G" first="Giovanni" last="Iliceto">Giovanni Iliceto</name><name sortKey="Livrea, Paolo" sort="Livrea, Paolo" uniqKey="Livrea P" first="Paolo" last="Livrea">Paolo Livrea</name><name sortKey="Zoccolella, Stefano" sort="Zoccolella, Stefano" uniqKey="Zoccolella S" first="Stefano" last="Zoccolella">Stefano Zoccolella</name></noCountry><country name="Italie"><noRegion><name 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