The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease
Identifieur interne : 000696 ( Main/Corpus ); précédent : 000695; suivant : 000697The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease
Auteurs : M. Białecka ; M. Dro Dzik ; G. Kłodowska-Duda ; K. Honczarenko ; B. Gawro Ska-Szklarz ; G. Opala ; J. StankiewiczSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 2004-10.
English descriptors
Abstract
Objectives – The etiology of sporadic idiopathic Parkinson's disease (PD) is considered multifactorial with both genetic and environmental factors modifying the disease expression. Recent studies suggest that polymorphism in monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) might influence the risk and treatment of PD. The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Materials and methods – A total of 95 patients (40 females and 55 males) of Polish origin diagnosed with sporadic PD were enrolled into the study, and were divided into two groups. Group 1 – patients treated with doses of levodopa below 500 mg/day during the first 5 years of treatment. Group 2 – patients requiring levodopa doses exceeding 500 mg/24 h during the first 5 years of treatment. Low activity alleles of MAOB and COMT, i.e. MAOB allele A and COMTL as well as high activity ones, i.e. MAOB allele G and COMTH, were determined using PCR‐RFLP method. Results – No statistically significant differences were found in MAOB and COMT allele distribution in the two groups. However, the frequency of COMTL/L homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. MAOB and COMT AG‐HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG‐LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h). Conclusion – The results of the study suggest that patients with COMTL/L genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.
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DOI: 10.1111/j.1600-0404.2004.00315.x
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease</title><author><name sortKey="Bialecka, M" sort="Bialecka, M" uniqKey="Bialecka M" first="M." last="Białecka">M. Białecka</name><affiliation><mods:affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Dro Dzik, M" sort="Dro Dzik, M" uniqKey="Dro Dzik M" first="M." last="Dro Dzik">M. Dro Dzik</name><affiliation><mods:affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Klodowska Uda, G" sort="Klodowska Uda, G" uniqKey="Klodowska Uda G" first="G." last="Kłodowska-Duda">G. Kłodowska-Duda</name><affiliation><mods:affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</mods:affiliation></affiliation></author><author><name sortKey="Honczarenko, K" sort="Honczarenko, K" uniqKey="Honczarenko K" first="K." last="Honczarenko">K. Honczarenko</name><affiliation><mods:affiliation>Department of Neurology, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Gawro Ska Zklarz, B" sort="Gawro Ska Zklarz, B" uniqKey="Gawro Ska Zklarz B" first="B." last="Gawro Ska-Szklarz">B. Gawro Ska-Szklarz</name><affiliation><mods:affiliation>Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Opala, G" sort="Opala, G" uniqKey="Opala G" first="G." last="Opala">G. Opala</name><affiliation><mods:affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</mods:affiliation></affiliation></author><author><name sortKey="Stankiewicz, J" sort="Stankiewicz, J" uniqKey="Stankiewicz J" first="J." last="Stankiewicz">J. Stankiewicz</name><affiliation><mods:affiliation>Department of Neurology, County Hospital, Szczecin, Poland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:F811DFDE2012B8521B68A96C48518236AE414DD8</idno><date when="2004" year="2004">2004</date><idno type="doi">10.1111/j.1600-0404.2004.00315.x</idno><idno type="url">https://api.istex.fr/document/F811DFDE2012B8521B68A96C48518236AE414DD8/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000696</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease</title><author><name sortKey="Bialecka, M" sort="Bialecka, M" uniqKey="Bialecka M" first="M." last="Białecka">M. Białecka</name><affiliation><mods:affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Dro Dzik, M" sort="Dro Dzik, M" uniqKey="Dro Dzik M" first="M." last="Dro Dzik">M. Dro Dzik</name><affiliation><mods:affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Klodowska Uda, G" sort="Klodowska Uda, G" uniqKey="Klodowska Uda G" first="G." last="Kłodowska-Duda">G. Kłodowska-Duda</name><affiliation><mods:affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</mods:affiliation></affiliation></author><author><name sortKey="Honczarenko, K" sort="Honczarenko, K" uniqKey="Honczarenko K" first="K." last="Honczarenko">K. Honczarenko</name><affiliation><mods:affiliation>Department of Neurology, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Gawro Ska Zklarz, B" sort="Gawro Ska Zklarz, B" uniqKey="Gawro Ska Zklarz B" first="B." last="Gawro Ska-Szklarz">B. Gawro Ska-Szklarz</name><affiliation><mods:affiliation>Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, Szczecin</mods:affiliation></affiliation></author><author><name sortKey="Opala, G" sort="Opala, G" uniqKey="Opala G" first="G." last="Opala">G. Opala</name><affiliation><mods:affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</mods:affiliation></affiliation></author><author><name sortKey="Stankiewicz, J" sort="Stankiewicz, J" uniqKey="Stankiewicz J" first="J." last="Stankiewicz">J. Stankiewicz</name><affiliation><mods:affiliation>Department of Neurology, County Hospital, Szczecin, Poland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neurologica Scandinavica</title><idno type="ISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2004-10">2004-10</date><biblScope unit="volume">110</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="260">260</biblScope><biblScope unit="page" to="266">266</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">F811DFDE2012B8521B68A96C48518236AE414DD8</idno><idno type="DOI">10.1111/j.1600-0404.2004.00315.x</idno><idno type="ArticleID">ANE315</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>catechol‐O‐methyltransferase</term><term>monoamine oxidase B</term><term>polymorphism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objectives – The etiology of sporadic idiopathic Parkinson's disease (PD) is considered multifactorial with both genetic and environmental factors modifying the disease expression. Recent studies suggest that polymorphism in monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) might influence the risk and treatment of PD. The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Materials and methods – A total of 95 patients (40 females and 55 males) of Polish origin diagnosed with sporadic PD were enrolled into the study, and were divided into two groups. Group 1 – patients treated with doses of levodopa below 500 mg/day during the first 5 years of treatment. Group 2 – patients requiring levodopa doses exceeding 500 mg/24 h during the first 5 years of treatment. Low activity alleles of MAOB and COMT, i.e. MAOB allele A and COMTL as well as high activity ones, i.e. MAOB allele G and COMTH, were determined using PCR‐RFLP method. Results – No statistically significant differences were found in MAOB and COMT allele distribution in the two groups. However, the frequency of COMTL/L homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. MAOB and COMT AG‐HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG‐LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h). Conclusion – The results of the study suggest that patients with COMTL/L genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>M. Białecka</name><affiliations><json:string>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</json:string></affiliations></json:item><json:item><name>M. Droździk</name><affiliations><json:string>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</json:string></affiliations></json:item><json:item><name>G. Kłodowska‐Duda</name><affiliations><json:string>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</json:string></affiliations></json:item><json:item><name>K. Honczarenko</name><affiliations><json:string>Department of Neurology, Pomeranian Medical University, Szczecin</json:string></affiliations></json:item><json:item><name>B. Gawrońska‐Szklarz</name><affiliations><json:string>Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, Szczecin</json:string></affiliations></json:item><json:item><name>G. Opala</name><affiliations><json:string>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</json:string></affiliations></json:item><json:item><name>J. Stankiewicz</name><affiliations><json:string>Department of Neurology, County Hospital, Szczecin, Poland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>catechol‐O‐methyltransferase</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>monoamine oxidase B</value></json:item><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>polymorphism</value></json:item></subject><articleId><json:string>ANE315</json:string></articleId><language><json:string>eng</json:string></language><abstract>Objectives – The etiology of sporadic idiopathic Parkinson's disease (PD) is considered multifactorial with both genetic and environmental factors modifying the disease expression. Recent studies suggest that polymorphism in monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) might influence the risk and treatment of PD. The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Materials and methods – A total of 95 patients (40 females and 55 males) of Polish origin diagnosed with sporadic PD were enrolled into the study, and were divided into two groups. Group 1 – patients treated with doses of levodopa below 500 mg/day during the first 5 years of treatment. Group 2 – patients requiring levodopa doses exceeding 500 mg/24 h during the first 5 years of treatment. Low activity alleles of MAOB and COMT, i.e. MAOB allele A and COMTL as well as high activity ones, i.e. MAOB allele G and COMTH, were determined using PCR‐RFLP method. Results – No statistically significant differences were found in MAOB and COMT allele distribution in the two groups. However, the frequency of COMTL/L homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. MAOB and COMT AG‐HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG‐LL haplotype in the group of females treated with low daily doses of levodopa (>500 mg/24 h). Conclusion – The results of the study suggest that patients with COMTL/L genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.</abstract><qualityIndicators><score>7.761</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 782 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>4</keywordCount><abstractCharCount>1880</abstractCharCount><pdfWordCount>4261</pdfWordCount><pdfCharCount>28015</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>291</abstractWordCount></qualityIndicators><title>The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's 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in patients with sporadic Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>2004</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease</title><author><persName><forename type="first">M.</forename><surname>Białecka</surname></persName><affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</affiliation></author><author><persName><forename type="first">M.</forename><surname>Droździk</surname></persName><affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</affiliation></author><author><persName><forename type="first">G.</forename><surname>Kłodowska‐Duda</surname></persName><affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</affiliation></author><author><persName><forename type="first">K.</forename><surname>Honczarenko</surname></persName><affiliation>Department of Neurology, Pomeranian Medical University, Szczecin</affiliation></author><author><persName><forename type="first">B.</forename><surname>Gawrońska‐Szklarz</surname></persName><affiliation>Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, Szczecin</affiliation></author><author><persName><forename type="first">G.</forename><surname>Opala</surname></persName><affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</affiliation></author><author><persName><forename type="first">J.</forename><surname>Stankiewicz</surname></persName><affiliation>Department of Neurology, County Hospital, Szczecin, Poland</affiliation></author></analytic><monogr><title level="j">Acta Neurologica Scandinavica</title><idno type="pISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><idno type="DOI">10.1111/(ISSN)1600-0404</idno><imprint><publisher>Munksgaard International Publishers</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2004-10"></date><biblScope unit="volume">110</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="260">260</biblScope><biblScope unit="page" to="266">266</biblScope></imprint></monogr><idno type="istex">F811DFDE2012B8521B68A96C48518236AE414DD8</idno><idno type="DOI">10.1111/j.1600-0404.2004.00315.x</idno><idno type="ArticleID">ANE315</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2004</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Objectives – The etiology of sporadic idiopathic Parkinson's disease (PD) is considered multifactorial with both genetic and environmental factors modifying the disease expression. Recent studies suggest that polymorphism in monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) might influence the risk and treatment of PD. The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Materials and methods – A total of 95 patients (40 females and 55 males) of Polish origin diagnosed with sporadic PD were enrolled into the study, and were divided into two groups. Group 1 – patients treated with doses of levodopa below 500 mg/day during the first 5 years of treatment. Group 2 – patients requiring levodopa doses exceeding 500 mg/24 h during the first 5 years of treatment. Low activity alleles of MAOB and COMT, i.e. MAOB allele A and COMTL as well as high activity ones, i.e. MAOB allele G and COMTH, were determined using PCR‐RFLP method. Results – No statistically significant differences were found in MAOB and COMT allele distribution in the two groups. However, the frequency of COMTL/L homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. MAOB and COMT AG‐HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG‐LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h). Conclusion – The results of the study suggest that patients with COMTL/L genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>catechol‐O‐methyltransferase</term></item><item><term>monoamine oxidase B</term></item><item><term>Parkinson's disease</term></item><item><term>polymorphism</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2004-10">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F811DFDE2012B8521B68A96C48518236AE414DD8/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>Munksgaard International Publishers</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1600-0404</doi><issn type="print">0001-6314</issn><issn type="electronic">1600-0404</issn><idGroup><id type="product" value="ANE"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="ACTA NEUROLOGICA SCANDINAVICA">Acta Neurologica Scandinavica</title></titleGroup></publicationMeta><publicationMeta level="part" position="10004"><doi origin="wiley">10.1111/ane.2004.110.issue-4</doi><numberingGroup><numbering type="journalVolume" number="110">110</numbering><numbering type="journalIssue" number="4">4</numbering></numberingGroup><coverDate startDate="2004-10">October 2004</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="8" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.2004.00315.x</doi><idGroup><id type="unit" value="ANE315"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><eventGroup><event type="firstOnline" date="2004-08-17"></event><event type="publishedOnlineFinalForm" date="2004-08-17"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-10"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:4.0.1" date="2014-03-15"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-14"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="260">260</numbering><numbering type="pageLast" number="266">266</numbering></numberingGroup><correspondenceTo>Dr Marek Drozdzik, Department of Pharmacology, Pomeranian Medical University, Powstancow Wlkp 72, 70‐111 Szczecin, Poland
Tel.: +4891‐4661589
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e‐mail: <email>drozdzik@sci.pam.szczecin.pl</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE315.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication May 11, 2004</unparsedEditorialHistory><countGroup><count type="figureTotal" number="0"></count><count type="tableTotal" number="4"></count></countGroup><titleGroup><title type="main">The effect of monoamine oxidase B (MAOB) and catechol‐<i>O</i>‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease</title><title type="shortAuthors"><b>Białecka et al.</b></title><title type="short"><b>Effect of MAOB and COMT polymorphisms on sporadic PD therapy with levodopa</b></title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>M.</givenNames><familyName>Białecka</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>M.</givenNames><familyName>Droździk</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>G.</givenNames><familyName>Kłodowska‐Duda</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a3"><personName><givenNames>K.</givenNames><familyName>Honczarenko</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a4"><personName><givenNames>B.</givenNames><familyName>Gawrońska‐Szklarz</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a2"><personName><givenNames>G.</givenNames><familyName>Opala</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a5"><personName><givenNames>J.</givenNames><familyName>Stankiewicz</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</unparsedAffiliation></affiliation><affiliation xml:id="a2"><unparsedAffiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Department of Neurology, Pomeranian Medical University, Szczecin</unparsedAffiliation></affiliation><affiliation xml:id="a4"><unparsedAffiliation>Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, Szczecin</unparsedAffiliation></affiliation><affiliation xml:id="a5" countryCode="PL"><unparsedAffiliation>Department of Neurology, County Hospital, Szczecin, Poland</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">catechol‐<i>O</i>‐methyltransferase</keyword><keyword xml:id="k2">monoamine oxidase B</keyword><keyword xml:id="k3">Parkinson's disease</keyword><keyword xml:id="k4">polymorphism</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><!-- Białecka M, Droździk M, Kłodowska-Duda G, Honczarenko K, Gawrońska-Szklarz B, Opala G, Stankiewicz J. The effect of monoamine oxidase B (MAOB) and catechol-O-methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease.
Acta Neurol Scand 2004 DOI: 10.1111/j.1600-0404.2004.00315.x © Blackwell Munksgaard 2004. --><p><b>Objectives – </b> The etiology of sporadic idiopathic Parkinson's disease (PD) is considered multifactorial with both genetic and environmental factors modifying the disease expression. Recent studies suggest that polymorphism in monoamine oxidase B (MAOB) and catechol‐<i>O</i>‐methyltransferase (COMT) might influence the risk and treatment of PD. The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations.</p><p><b>Materials and methods – </b> A total of 95 patients (40 females and 55 males) of Polish origin diagnosed with sporadic PD were enrolled into the study, and were divided into two groups. Group 1 – patients treated with doses of levodopa below 500 mg/day during the first 5 years of treatment. Group 2 – patients requiring levodopa doses exceeding 500 mg/24 h during the first 5 years of treatment. Low activity alleles of MAOB and COMT, i.e. MAOB allele A and COMT<sup>L</sup> as well as high activity ones, i.e. MAOB allele G and COMT<sup>H</sup>, were determined using PCR‐RFLP method.</p><p><b>Results – </b> No statistically significant differences were found in MAOB and COMT allele distribution in the two groups. However, the frequency of COMT<sup>L/L</sup> homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. MAOB and COMT AG‐HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG‐LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h).</p><p><b>Conclusion – </b> The results of the study suggest that patients with COMT<sup>L/L</sup> genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>The effect of monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) polymorphisms on levodopa therapy in patients with sporadic Parkinson's disease</title></titleInfo><titleInfo type="abbreviated"><title>Effect of MAOB and COMT polymorphisms on sporadic PD therapy with levodopa</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>The effect of monoamine oxidase B (MAOB) and catechol‐</title></titleInfo><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Białecka</namePart><affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Droździk</namePart><affiliation>Department of Experimental and Clinical Pharmacology, Pomeranian Medical University, Szczecin</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Kłodowska‐Duda</namePart><affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">K.</namePart><namePart type="family">Honczarenko</namePart><affiliation>Department of Neurology, Pomeranian Medical University, Szczecin</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">B.</namePart><namePart type="family">Gawrońska‐Szklarz</namePart><affiliation>Department of Pharmacokinetics and Therapeutic Drug Monitoring, Pomeranian Medical University, Szczecin</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Opala</namePart><affiliation>Department of Neurology, Ageing Degenerative and Cerebrovascular Diseases, Medical University of Silesia, Katowice</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">J.</namePart><namePart type="family">Stankiewicz</namePart><affiliation>Department of Neurology, County Hospital, Szczecin, Poland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Munksgaard International Publishers</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2004-10</dateIssued><edition>Accepted for publication May 11, 2004</edition><copyrightDate encoding="w3cdtf">2004</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="tables">4</extent></physicalDescription><abstract lang="en">Objectives – The etiology of sporadic idiopathic Parkinson's disease (PD) is considered multifactorial with both genetic and environmental factors modifying the disease expression. Recent studies suggest that polymorphism in monoamine oxidase B (MAOB) and catechol‐O‐methyltransferase (COMT) might influence the risk and treatment of PD. The aim of the study was to evaluate the effect of MAOB and COMT genetic polymorphism on effective daily dose of levodopa applied during the first 5 years of treatment, and to find out if a relationship exists between MAOB and COMT haplotypes and motor disturbances onset in PD patients treated with levodopa preparations. Materials and methods – A total of 95 patients (40 females and 55 males) of Polish origin diagnosed with sporadic PD were enrolled into the study, and were divided into two groups. Group 1 – patients treated with doses of levodopa below 500 mg/day during the first 5 years of treatment. Group 2 – patients requiring levodopa doses exceeding 500 mg/24 h during the first 5 years of treatment. Low activity alleles of MAOB and COMT, i.e. MAOB allele A and COMTL as well as high activity ones, i.e. MAOB allele G and COMTH, were determined using PCR‐RFLP method. Results – No statistically significant differences were found in MAOB and COMT allele distribution in the two groups. However, the frequency of COMTL/L homozygotes was higher in the group treated with low doses of levodopa when compared with the second group. MAOB and COMT AG‐HH haplotype predominated in the group of females treated with high daily doses of levodopa when compared with AG‐LL haplotype in the group of females treated with low daily doses of levodopa (<500 mg/24 h). Conclusion – The results of the study suggest that patients with COMTL/L genotype and possibly MAOB genotype A may benefit from more efficient and safer levodopa therapy.</abstract><subject lang="en"><genre>Keywords</genre><topic>catechol‐O‐methyltransferase</topic><topic>monoamine oxidase B</topic><topic>Parkinson's disease</topic><topic>polymorphism</topic></subject><relatedItem type="host"><titleInfo><title>Acta Neurologica Scandinavica</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0001-6314</identifier><identifier type="eISSN">1600-0404</identifier><identifier type="DOI">10.1111/(ISSN)1600-0404</identifier><identifier type="PublisherID">ANE</identifier><part><date>2004</date><detail type="volume"><caption>vol.</caption><number>110</number></detail><detail type="issue"><caption>no.</caption><number>4</number></detail><extent unit="pages"><start>260</start><end>266</end><total>7</total></extent></part></relatedItem><identifier type="istex">F811DFDE2012B8521B68A96C48518236AE414DD8</identifier><identifier type="DOI">10.1111/j.1600-0404.2004.00315.x</identifier><identifier type="ArticleID">ANE315</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Munksgaard International Publishers</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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