Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients
Identifieur interne : 002A07 ( Istex/Corpus ); précédent : 002A06; suivant : 002A08Effects 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 ] ; 2005-01.
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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. © 2004 Movement Disorder Society
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DOI: 10.1002/mds.20261
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ISTEX:059344931BC5E86B701FB0820B8FB0F10271CDBELe document en format XML
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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="2005-01">2005-01</date><biblScope unit="vol">20</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="69">69</biblScope><biblScope unit="page" to="72">72</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">059344931BC5E86B701FB0820B8FB0F10271CDBE</idno><idno type="DOI">10.1002/mds.20261</idno><idno type="ArticleID">MDS20261</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>COMT inhibitors</term><term>Parkinson's disease</term><term>homocysteine</term><term>levodopa</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></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. © 2004 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Paolo Lamberti MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bari, Bari, Italy</json:string></affiliations></json:item><json:item><name>Stefano Zoccolella MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bari, Bari, Italy</json:string></affiliations></json:item><json:item><name>Giovanni Iliceto MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bari, Bari, Italy</json:string></affiliations></json:item><json:item><name>Elio Armenise MD</name><affiliations><json:string>Department of Internal Medicine and Public Health‐Hygiene Section, University of Bari, Bari, Italy</json:string></affiliations></json:item><json:item><name>Angela Fraddosio MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bari, Bari, Italy</json:string></affiliations></json:item><json:item><name>Michele De Mari MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bari, Bari, Italy</json:string></affiliations></json:item><json:item><name>Paolo Livrea MD</name><affiliations><json:string>Department of Neurological Sciences, University of Bari, Bari, Italy</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>homocysteine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>levodopa</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>COMT inhibitors</value></json:item></subject><language><json:string>eng</json:string></language><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. 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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. © 2004 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>homocysteine</term></item><item><term>levodopa</term></item><item><term>COMT inhibitors</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Brief Report</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2003-12-03">Received</change><change when="2004-03-09">Registration</change><change when="2005-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/059344931BC5E86B701FB0820B8FB0F10271CDBE/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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Cesare 11, 70124 Bari, Italy</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS20261.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="1"></count><count type="tableTotal" number="1"></count><count type="referenceTotal" number="16"></count><count type="wordTotal" number="2438"></count></countGroup><titleGroup><title type="main" xml:lang="en">Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients</title><title type="short" xml:lang="en"><sc>L</sc>‐DOPA, COMT Inhibitors, and Homocysteine in PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Paolo</givenNames><familyName>Lamberti</familyName><degrees>MD</degrees></personName><contactDetails><email>lamberti@neurol.uniba.it</email></contactDetails></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Stefano</givenNames><familyName>Zoccolella</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Giovanni</givenNames><familyName>Iliceto</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Elio</givenNames><familyName>Armenise</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Angela</givenNames><familyName>Fraddosio</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au6" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michele</givenNames><familyName>De Mari</familyName><degrees>MD</degrees></personName></creator><creator xml:id="au7" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Paolo</givenNames><familyName>Livrea</familyName><degrees>MD</degrees></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IT" type="organization"><unparsedAffiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="IT" type="organization"><unparsedAffiliation>Department of Internal Medicine and Public Health‐Hygiene Section, University of Bari, Bari, Italy</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Parkinson's disease</keyword><keyword xml:id="kwd2">homocysteine</keyword><keyword xml:id="kwd3">levodopa</keyword><keyword xml:id="kwd4">COMT inhibitors</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>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‐<i>O</i>‐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. © 2004 Movement Disorder Society</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 4-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>L‐DOPA, COMT Inhibitors, and Homocysteine in PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Effects of levodopa and COMT inhibitors on plasma homocysteine in Parkinson's disease patients</title></titleInfo><name type="personal"><namePart type="given">Paolo</namePart><namePart type="family">Lamberti</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</affiliation><description>Correspondence: Department of Neurological Sciences, University of Bari, Ospedale Policlinico, P.zza G. Cesare 11, 70124 Bari, Italy</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Stefano</namePart><namePart type="family">Zoccolella</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Giovanni</namePart><namePart type="family">Iliceto</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Elio</namePart><namePart type="family">Armenise</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Internal Medicine and Public Health‐Hygiene Section, University of Bari, Bari, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Angela</namePart><namePart type="family">Fraddosio</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michele</namePart><namePart type="family">De Mari</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Paolo</namePart><namePart type="family">Livrea</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurological Sciences, University of Bari, Bari, Italy</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2005-01</dateIssued><dateCaptured encoding="w3cdtf">2003-12-03</dateCaptured><dateValid encoding="w3cdtf">2004-03-09</dateValid><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">1</extent><extent unit="tables">1</extent><extent unit="references">16</extent><extent unit="words">2438</extent></physicalDescription><abstract 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. © 2004 Movement Disorder Society</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>homocysteine</topic><topic>levodopa</topic><topic>COMT inhibitors</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Brief Report</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>20</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>69</start><end>72</end><total>4</total></extent></part></relatedItem><identifier type="istex">059344931BC5E86B701FB0820B8FB0F10271CDBE</identifier><identifier type="DOI">10.1002/mds.20261</identifier><identifier type="ArticleID">MDS20261</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2004 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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