Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease
Identifieur interne : 000381 ( Istex/Corpus ); précédent : 000380; suivant : 000382Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease
Auteurs : Lyytinen ; Seppo Kaakkola ; Sirpa Ahtila ; P Ivi Tuomainen ; Heikki Ter V InenSource :
- Movement Disorders [ 0885-3185 ] ; 1997-07.
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- KwdEn :
Abstract
The effect of selegiline (L‐deprenyl) on plasma catecholamines, clinical response, and drug tolerability was studied in 13 patients with Parkinson's disease (PD) treated with L‐Dopa/benserazide and entacapone, a peripheral catechol‐O‐methyltransferase (COMT) inhibitor, in a placebo‐controlled double‐blind study. An L‐Dopa test was performed on 3 study days. The first study day was with L‐Dopa/benserazide only (control), the second after 14 days of treatment with 200 mg entacapone taken concomitantly with L‐Dopa/benserazide in combination with either selegiline (10 mg daily) or placebo. After a 2‐week washout period, selegiline and placebo treatments were switched, and the third study day was after 14 days of treatment. During the study days, clinical response was evaluated at 30‐min intervals for 6 h, by using the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS). In addition, repeated blood pressure measurements were made, and plasma samples were taken for analysis of L‐Dopa, 3‐O‐methyldopa (3‐OMD), dihydroxyphenyl acetic acid (DOPAC), homovanillic acid (HVA), dopamine, nor‐adrenaline, and 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG). Monoamine oxidase B (MAO‐B) and COMT enzyme activities were measured from platelets and erythrocytes, respectively. Entacapone improved the clinical response to L‐Dopa during both selegiline and placebo (p < 0.001) treatments. The improvement was more marked during combined selegiline and entacapone treatment than with entacapone alone (p < 0.01). Entacapone significantly increased plasma L‐Dopa and DOPAC levels and decreased plasma 3‐OMD and MHPG levels both with selegiline and placebo. Selegiline partially inhibited the entacapone‐induced increase of plasma DOPAC. Plasma dopamine and noradrenaline levels did not change. Entacapone decreased erythrocyte COMT activity by >35% (p < 0.001), and platelet MAO‐B activity was almost completely inhibited by selegiline (p < 0.001). One patient withdrew because of diarrhea, dizziness, and loss of sleep when receiving selegiline treatment. Otherwise no differences in adverse events, mean daily blood pressures, or other safety parameters were observed between selegiline and placebo treatments. Our results suggest that entacapone can be safely administered together with L‐Dopa and selegiline in patients with PD, although further studies with larger number of patients and longer treatment periods are necessary to confirm this finding.
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DOI: 10.1002/mds.870120404
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<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease</title><author><name sortKey="Lyytinen" sort="Lyytinen" uniqKey="Lyytinen" last="Lyytinen">Lyytinen</name><affiliation><mods:affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Kaakkola, Seppo" sort="Kaakkola, Seppo" uniqKey="Kaakkola S" first="Seppo" last="Kaakkola">Seppo Kaakkola</name><affiliation><mods:affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Ahtila, Sirpa" sort="Ahtila, Sirpa" uniqKey="Ahtila S" first="Sirpa" last="Ahtila">Sirpa Ahtila</name><affiliation><mods:affiliation>National Agency for Medicines, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Tuomainen, P Ivi" sort="Tuomainen, P Ivi" uniqKey="Tuomainen P" first="P Ivi" last="Tuomainen">P Ivi Tuomainen</name><affiliation><mods:affiliation>Department of Pharmacology and Toxicology, University of Helsinki, Helsinki, Finland.</mods:affiliation></affiliation></author><author><name sortKey="Ter V Inen, Heikki" sort="Ter V Inen, Heikki" uniqKey="Ter V Inen H" first="Heikki" last="Ter V Inen">Heikki Ter V Inen</name><affiliation><mods:affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1002/mds.870120404</idno><idno type="url">https://api.istex.fr/document/6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000381</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease</title><author><name sortKey="Lyytinen" sort="Lyytinen" uniqKey="Lyytinen" last="Lyytinen">Lyytinen</name><affiliation><mods:affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Kaakkola, Seppo" sort="Kaakkola, Seppo" uniqKey="Kaakkola S" first="Seppo" last="Kaakkola">Seppo Kaakkola</name><affiliation><mods:affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Ahtila, Sirpa" sort="Ahtila, Sirpa" uniqKey="Ahtila S" first="Sirpa" last="Ahtila">Sirpa Ahtila</name><affiliation><mods:affiliation>National Agency for Medicines, University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author><author><name sortKey="Tuomainen, P Ivi" sort="Tuomainen, P Ivi" uniqKey="Tuomainen P" first="P Ivi" last="Tuomainen">P Ivi Tuomainen</name><affiliation><mods:affiliation>Department of Pharmacology and Toxicology, University of Helsinki, Helsinki, Finland.</mods:affiliation></affiliation></author><author><name sortKey="Ter V Inen, Heikki" sort="Ter V Inen, Heikki" uniqKey="Ter V Inen H" first="Heikki" last="Ter V Inen">Heikki Ter V Inen</name><affiliation><mods:affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="1997-07">1997-07</date><biblScope unit="vol">12</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="497">497</biblScope><biblScope unit="page" to="505">505</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D</idno><idno type="DOI">10.1002/mds.870120404</idno><idno type="ArticleID">MDS870120404</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>COMT</term><term>Catecholamines</term><term>Entacapone</term><term>MAO‐B</term><term>Parkinson's disease</term><term>Selegiline</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The effect of selegiline (L‐deprenyl) on plasma catecholamines, clinical response, and drug tolerability was studied in 13 patients with Parkinson's disease (PD) treated with L‐Dopa/benserazide and entacapone, a peripheral catechol‐O‐methyltransferase (COMT) inhibitor, in a placebo‐controlled double‐blind study. An L‐Dopa test was performed on 3 study days. The first study day was with L‐Dopa/benserazide only (control), the second after 14 days of treatment with 200 mg entacapone taken concomitantly with L‐Dopa/benserazide in combination with either selegiline (10 mg daily) or placebo. After a 2‐week washout period, selegiline and placebo treatments were switched, and the third study day was after 14 days of treatment. During the study days, clinical response was evaluated at 30‐min intervals for 6 h, by using the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS). In addition, repeated blood pressure measurements were made, and plasma samples were taken for analysis of L‐Dopa, 3‐O‐methyldopa (3‐OMD), dihydroxyphenyl acetic acid (DOPAC), homovanillic acid (HVA), dopamine, nor‐adrenaline, and 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG). Monoamine oxidase B (MAO‐B) and COMT enzyme activities were measured from platelets and erythrocytes, respectively. Entacapone improved the clinical response to L‐Dopa during both selegiline and placebo (p < 0.001) treatments. The improvement was more marked during combined selegiline and entacapone treatment than with entacapone alone (p < 0.01). Entacapone significantly increased plasma L‐Dopa and DOPAC levels and decreased plasma 3‐OMD and MHPG levels both with selegiline and placebo. Selegiline partially inhibited the entacapone‐induced increase of plasma DOPAC. Plasma dopamine and noradrenaline levels did not change. Entacapone decreased erythrocyte COMT activity by >35% (p < 0.001), and platelet MAO‐B activity was almost completely inhibited by selegiline (p < 0.001). One patient withdrew because of diarrhea, dizziness, and loss of sleep when receiving selegiline treatment. Otherwise no differences in adverse events, mean daily blood pressures, or other safety parameters were observed between selegiline and placebo treatments. Our results suggest that entacapone can be safely administered together with L‐Dopa and selegiline in patients with PD, although further studies with larger number of patients and longer treatment periods are necessary to confirm this finding.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Dr. Lyytinen</name><affiliations><json:string>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Seppo Kaakkola</name><affiliations><json:string>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Sirpa Ahtila</name><affiliations><json:string>National Agency for Medicines, University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item><json:item><name>Päivi Tuomainen</name><affiliations><json:string>Department of Pharmacology and Toxicology, University of Helsinki, Helsinki, Finland.</json:string></affiliations></json:item><json:item><name>Heikki Teräväinen</name><affiliations><json:string>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Entacapone</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Selegiline</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Catecholamines</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>COMT</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MAO‐B</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The effect of selegiline (L‐deprenyl) on plasma catecholamines, clinical response, and drug tolerability was studied in 13 patients with Parkinson's disease (PD) treated with L‐Dopa/benserazide and entacapone, a peripheral catechol‐O‐methyltransferase (COMT) inhibitor, in a placebo‐controlled double‐blind study. An L‐Dopa test was performed on 3 study days. The first study day was with L‐Dopa/benserazide only (control), the second after 14 days of treatment with 200 mg entacapone taken concomitantly with L‐Dopa/benserazide in combination with either selegiline (10 mg daily) or placebo. After a 2‐week washout period, selegiline and placebo treatments were switched, and the third study day was after 14 days of treatment. During the study days, clinical response was evaluated at 30‐min intervals for 6 h, by using the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS). In addition, repeated blood pressure measurements were made, and plasma samples were taken for analysis of L‐Dopa, 3‐O‐methyldopa (3‐OMD), dihydroxyphenyl acetic acid (DOPAC), homovanillic acid (HVA), dopamine, nor‐adrenaline, and 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG). Monoamine oxidase B (MAO‐B) and COMT enzyme activities were measured from platelets and erythrocytes, respectively. Entacapone improved the clinical response to L‐Dopa during both selegiline and placebo (p > 0.001) treatments. The improvement was more marked during combined selegiline and entacapone treatment than with entacapone alone (p > 0.01). Entacapone significantly increased plasma L‐Dopa and DOPAC levels and decreased plasma 3‐OMD and MHPG levels both with selegiline and placebo. Selegiline partially inhibited the entacapone‐induced increase of plasma DOPAC. Plasma dopamine and noradrenaline levels did not change. Entacapone decreased erythrocyte COMT activity by >35% (p > 0.001), and platelet MAO‐B activity was almost completely inhibited by selegiline (p > 0.001). One patient withdrew because of diarrhea, dizziness, and loss of sleep when receiving selegiline treatment. Otherwise no differences in adverse events, mean daily blood pressures, or other safety parameters were observed between selegiline and placebo treatments. Our results suggest that entacapone can be safely administered together with L‐Dopa and selegiline in patients with PD, although further studies with larger number of patients and longer treatment periods are necessary to confirm this finding.</abstract><qualityIndicators><score>7.672</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 827.759 pts</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>2467</abstractCharCount><pdfWordCount>4672</pdfWordCount><pdfCharCount>30498</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>342</abstractWordCount></qualityIndicators><title>Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease</title><genre><json:string>Serial article</json:string></genre><host><volume>12</volume><pages><total>9</total><last>505</last><first>497</first></pages><issn><json:string>0885-3185</json:string></issn><issue>4</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1997</publicationDate><copyrightDate>1997</copyrightDate><doi><json:string>10.1002/mds.870120404</json:string></doi><id>6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1997</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease</title><author><persName><surname>Lyytinen</surname><roleName type="degree">Dr.</roleName></persName><note type="correspondence"><p>Correspondence: Department of Neurology, University of Helsinki, Haartmaninkatu 4, FIN‐00290 Helsinki, Finland</p></note><affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</affiliation></author><author><persName><forename type="first">Seppo</forename><surname>Kaakkola</surname></persName><affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</affiliation></author><author><persName><forename type="first">Sirpa</forename><surname>Ahtila</surname></persName><affiliation>National Agency for Medicines, University of Helsinki, Helsinki, Finland</affiliation></author><author><persName><forename type="first">Päivi</forename><surname>Tuomainen</surname></persName><affiliation>Department of Pharmacology and Toxicology, University of Helsinki, Helsinki, Finland.</affiliation></author><author><persName><forename type="first">Heikki</forename><surname>Teräväinen</surname></persName><affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1997-07"></date><biblScope unit="vol">12</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="497">497</biblScope><biblScope unit="page" to="505">505</biblScope></imprint></monogr><idno type="istex">6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D</idno><idno type="DOI">10.1002/mds.870120404</idno><idno type="ArticleID">MDS870120404</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The effect of selegiline (L‐deprenyl) on plasma catecholamines, clinical response, and drug tolerability was studied in 13 patients with Parkinson's disease (PD) treated with L‐Dopa/benserazide and entacapone, a peripheral catechol‐O‐methyltransferase (COMT) inhibitor, in a placebo‐controlled double‐blind study. An L‐Dopa test was performed on 3 study days. The first study day was with L‐Dopa/benserazide only (control), the second after 14 days of treatment with 200 mg entacapone taken concomitantly with L‐Dopa/benserazide in combination with either selegiline (10 mg daily) or placebo. After a 2‐week washout period, selegiline and placebo treatments were switched, and the third study day was after 14 days of treatment. During the study days, clinical response was evaluated at 30‐min intervals for 6 h, by using the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS). In addition, repeated blood pressure measurements were made, and plasma samples were taken for analysis of L‐Dopa, 3‐O‐methyldopa (3‐OMD), dihydroxyphenyl acetic acid (DOPAC), homovanillic acid (HVA), dopamine, nor‐adrenaline, and 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG). Monoamine oxidase B (MAO‐B) and COMT enzyme activities were measured from platelets and erythrocytes, respectively. Entacapone improved the clinical response to L‐Dopa during both selegiline and placebo (p < 0.001) treatments. The improvement was more marked during combined selegiline and entacapone treatment than with entacapone alone (p < 0.01). Entacapone significantly increased plasma L‐Dopa and DOPAC levels and decreased plasma 3‐OMD and MHPG levels both with selegiline and placebo. Selegiline partially inhibited the entacapone‐induced increase of plasma DOPAC. Plasma dopamine and noradrenaline levels did not change. Entacapone decreased erythrocyte COMT activity by >35% (p < 0.001), and platelet MAO‐B activity was almost completely inhibited by selegiline (p < 0.001). One patient withdrew because of diarrhea, dizziness, and loss of sleep when receiving selegiline treatment. Otherwise no differences in adverse events, mean daily blood pressures, or other safety parameters were observed between selegiline and placebo treatments. Our results suggest that entacapone can be safely administered together with L‐Dopa and selegiline in patients with PD, although further studies with larger number of patients and longer treatment periods are necessary to confirm this finding.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Entacapone</term></item><item><term>Selegiline</term></item><item><term>Catecholamines</term></item><item><term>COMT</term></item><item><term>MAO‐B</term></item><item><term>Parkinson's disease</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1996-01-19">Received</change><change when="1996-10-07">Registration</change><change when="1997-07">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/6F7F2D5338FF9BFE1C92834EF57EA9AAA2D0278D/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. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="40"><doi origin="wiley" registered="yes">10.1002/mds.v12:4</doi><numberingGroup><numbering type="journalVolume" number="12">12</numbering><numbering type="journalIssue">4</numbering></numberingGroup><coverDate startDate="1997-07">July 1997</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870120404</doi><idGroup><id type="unit" value="MDS870120404"></id></idGroup><countGroup><count type="pageTotal" number="9"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1997 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1996-01-19"></event><event type="manuscriptRevised" date="1996-08-01"></event><event type="manuscriptAccepted" date="1996-10-07"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">497</numbering><numbering type="pageLast">505</numbering></numberingGroup><correspondenceTo>Department of Neurology, University of Helsinki, Haartmaninkatu 4, FIN‐00290 Helsinki, Finland</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870120404.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="4"></count><count type="tableTotal" number="4"></count><count type="referenceTotal" number="30"></count></countGroup><titleGroup><title type="main" xml:lang="en">Simultaneous MAO‐B and COMT inhibition in <sc>L</sc>‐dopa‐treated patients with parkinson's disease</title><title type="short" xml:lang="en">MAO‐B AND COMT INHIBITION IN PD</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><honorifics>Dr.</honorifics><givenNames>Jukka</givenNames><familyName>Lyytinen</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Seppo</givenNames><familyName>Kaakkola</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af2"><personName><givenNames>Sirpa</givenNames><familyName>Ahtila</familyName></personName></creator><creator xml:id="au4" creatorRole="author" affiliationRef="#af3"><personName><givenNames>Päivi</givenNames><familyName>Tuomainen</familyName></personName></creator><creator xml:id="au5" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Heikki</givenNames><familyName>Teräväinen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="FI" type="organization"><unparsedAffiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af2" countryCode="FI" type="organization"><unparsedAffiliation>National Agency for Medicines, University of Helsinki, Helsinki, Finland</unparsedAffiliation></affiliation><affiliation xml:id="af3" countryCode="FI" type="organization"><unparsedAffiliation>Department of Pharmacology and Toxicology, University of Helsinki, Helsinki, Finland.</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Entacapone</keyword><keyword xml:id="kwd2">Selegiline</keyword><keyword xml:id="kwd3">Catecholamines</keyword><keyword xml:id="kwd4">COMT</keyword><keyword xml:id="kwd5">MAO‐B</keyword><keyword xml:id="kwd6">Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>The effect of selegiline (<sc>L</sc>‐deprenyl) on plasma catecholamines, clinical response, and drug tolerability was studied in 13 patients with Parkinson's disease (PD) treated with <sc>L</sc>‐Dopa/benserazide and entacapone, a peripheral catechol‐<i>O</i>‐methyltransferase (COMT) inhibitor, in a placebo‐controlled double‐blind study. An <sc>L</sc>‐Dopa test was performed on 3 study days. The first study day was with <sc>L</sc>‐Dopa/benserazide only (control), the second after 14 days of treatment with 200 mg entacapone taken concomitantly with <sc>L</sc>‐Dopa/benserazide in combination with either selegiline (10 mg daily) or placebo. After a 2‐week washout period, selegiline and placebo treatments were switched, and the third study day was after 14 days of treatment. During the study days, clinical response was evaluated at 30‐min intervals for 6 h, by using the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS). In addition, repeated blood pressure measurements were made, and plasma samples were taken for analysis of <sc>L</sc>‐Dopa, 3‐<i>O</i>‐methyldopa (3‐OMD), dihydroxyphenyl acetic acid (DOPAC), homovanillic acid (HVA), dopamine, nor‐adrenaline, and 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG). Monoamine oxidase B (MAO‐B) and COMT enzyme activities were measured from platelets and erythrocytes, respectively. Entacapone improved the clinical response to <sc>L</sc>‐Dopa during both selegiline and placebo (p < 0.001) treatments. The improvement was more marked during combined selegiline and entacapone treatment than with entacapone alone (p < 0.01). Entacapone significantly increased plasma <sc>L</sc>‐Dopa and DOPAC levels and decreased plasma 3‐OMD and MHPG levels both with selegiline and placebo. Selegiline partially inhibited the entacapone‐induced increase of plasma DOPAC. Plasma dopamine and noradrenaline levels did not change. Entacapone decreased erythrocyte COMT activity by >35% (p < 0.001), and platelet MAO‐B activity was almost completely inhibited by selegiline (p < 0.001). One patient withdrew because of diarrhea, dizziness, and loss of sleep when receiving selegiline treatment. Otherwise no differences in adverse events, mean daily blood pressures, or other safety parameters were observed between selegiline and placebo treatments. Our results suggest that entacapone can be safely administered together with <sc>L</sc>‐Dopa and selegiline in patients with PD, although further studies with larger number of patients and longer treatment periods are necessary to confirm this finding.</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>Simultaneous MAO‐B and COMT inhibition in L‐dopa‐treated patients with parkinson's disease</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>MAO‐B AND COMT INHIBITION IN PD</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Simultaneous MAO‐B and COMT inhibition in</title></titleInfo><name type="personal"><namePart type="termsOfAddress">Dr.</namePart><namePart type="family">Lyytinen</namePart><affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</affiliation><description>Correspondence: Department of Neurology, University of Helsinki, Haartmaninkatu 4, FIN‐00290 Helsinki, Finland</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seppo</namePart><namePart type="family">Kaakkola</namePart><affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sirpa</namePart><namePart type="family">Ahtila</namePart><affiliation>National Agency for Medicines, University of Helsinki, Helsinki, Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Päivi</namePart><namePart type="family">Tuomainen</namePart><affiliation>Department of Pharmacology and Toxicology, University of Helsinki, Helsinki, Finland.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Heikki</namePart><namePart type="family">Teräväinen</namePart><affiliation>Department of Neurology, University of Helsinki; University of Helsinki, Helsinki, Finland</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">1997-07</dateIssued><dateCaptured encoding="w3cdtf">1996-01-19</dateCaptured><dateValid encoding="w3cdtf">1996-10-07</dateValid><copyrightDate encoding="w3cdtf">1997</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">4</extent><extent unit="tables">4</extent><extent unit="references">30</extent></physicalDescription><abstract lang="en">The effect of selegiline (L‐deprenyl) on plasma catecholamines, clinical response, and drug tolerability was studied in 13 patients with Parkinson's disease (PD) treated with L‐Dopa/benserazide and entacapone, a peripheral catechol‐O‐methyltransferase (COMT) inhibitor, in a placebo‐controlled double‐blind study. An L‐Dopa test was performed on 3 study days. The first study day was with L‐Dopa/benserazide only (control), the second after 14 days of treatment with 200 mg entacapone taken concomitantly with L‐Dopa/benserazide in combination with either selegiline (10 mg daily) or placebo. After a 2‐week washout period, selegiline and placebo treatments were switched, and the third study day was after 14 days of treatment. During the study days, clinical response was evaluated at 30‐min intervals for 6 h, by using the motor score of the Unified Parkinson's Disease Rating Scale (UPDRS). In addition, repeated blood pressure measurements were made, and plasma samples were taken for analysis of L‐Dopa, 3‐O‐methyldopa (3‐OMD), dihydroxyphenyl acetic acid (DOPAC), homovanillic acid (HVA), dopamine, nor‐adrenaline, and 3‐methoxy‐4‐hydroxyphenylethylene glycol (MHPG). Monoamine oxidase B (MAO‐B) and COMT enzyme activities were measured from platelets and erythrocytes, respectively. Entacapone improved the clinical response to L‐Dopa during both selegiline and placebo (p < 0.001) treatments. The improvement was more marked during combined selegiline and entacapone treatment than with entacapone alone (p < 0.01). Entacapone significantly increased plasma L‐Dopa and DOPAC levels and decreased plasma 3‐OMD and MHPG levels both with selegiline and placebo. Selegiline partially inhibited the entacapone‐induced increase of plasma DOPAC. Plasma dopamine and noradrenaline levels did not change. Entacapone decreased erythrocyte COMT activity by >35% (p < 0.001), and platelet MAO‐B activity was almost completely inhibited by selegiline (p < 0.001). One patient withdrew because of diarrhea, dizziness, and loss of sleep when receiving selegiline treatment. Otherwise no differences in adverse events, mean daily blood pressures, or other safety parameters were observed between selegiline and placebo treatments. Our results suggest that entacapone can be safely administered together with L‐Dopa and selegiline in patients with PD, although further studies with larger number of patients and longer treatment periods are necessary to confirm this finding.</abstract><subject lang="en"><genre>Keywords</genre><topic>Entacapone</topic><topic>Selegiline</topic><topic>Catecholamines</topic><topic>COMT</topic><topic>MAO‐B</topic><topic>Parkinson's disease</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. 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