Tetrahydrobiopterin and Parkinson's disease
Identifieur interne : 002F51 ( Main/Corpus ); précédent : 002F50; suivant : 002F52Tetrahydrobiopterin and Parkinson's disease
Auteurs : I. C. Dissing ; F. Güttler ; H. Pakkenberg ; H. Lou ; A. Gerdes ; C. Lykkelund ; V. RasmussenSource :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 1989-06.
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- KwdEn :
Abstract
ABSTRACT— Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH4) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4–8 fold increase in the concentration of homovanillic acid (HVA), and a 3‐fold increase in the concentration of 5‐hydroxyindole acetic acid (5‐HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13–37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH4 administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH4 in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5‐HIAA was observed. The results suggest, the BH4 in the dosage used, is not effective in the treatment of Parkinson's disease.
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DOI: 10.1111/j.1600-0404.1989.tb03820.x
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ISTEX:7655FDDCDF51677613CAF8FD228677B80485252ALe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Tetrahydrobiopterin and Parkinson's disease</title><author><name sortKey="Dissing, I C" sort="Dissing, I C" uniqKey="Dissing I" first="I. C." last="Dissing">I. C. Dissing</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Guttler, F" sort="Guttler, F" uniqKey="Guttler F" first="F." last="Güttler">F. Güttler</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Pakkenberg, H" sort="Pakkenberg, H" uniqKey="Pakkenberg H" first="H." last="Pakkenberg">H. Pakkenberg</name><affiliation><mods:affiliation>Department of Neurology, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Lou, H" sort="Lou, H" uniqKey="Lou H" first="H." last="Lou">H. Lou</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Gerdes, A" sort="Gerdes, A" uniqKey="Gerdes A" first="A." last="Gerdes">A. Gerdes</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Lykkelund, C" sort="Lykkelund, C" uniqKey="Lykkelund C" first="C." last="Lykkelund">C. Lykkelund</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Rasmussen, V" sort="Rasmussen, V" uniqKey="Rasmussen V" first="V." last="Rasmussen">V. 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Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Lykkelund, C" sort="Lykkelund, C" uniqKey="Lykkelund C" first="C." last="Lykkelund">C. Lykkelund</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</mods:affiliation></affiliation></author><author><name sortKey="Rasmussen, V" sort="Rasmussen, V" uniqKey="Rasmussen V" first="V." last="Rasmussen">V. Rasmussen</name><affiliation><mods:affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</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>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1989-06">1989-06</date><biblScope unit="volume">79</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="493">493</biblScope><biblScope unit="page" to="499">499</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">7655FDDCDF51677613CAF8FD228677B80485252A</idno><idno type="DOI">10.1111/j.1600-0404.1989.tb03820.x</idno><idno type="ArticleID">ANE493</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>5‐HIAA</term><term>HVA</term><term>Parkinson's disease</term><term>biopterin</term><term>dopamine</term><term>phenylalanine</term><term>serotonin</term><term>tryptophan</term><term>tyrosine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">ABSTRACT— Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH4) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4–8 fold increase in the concentration of homovanillic acid (HVA), and a 3‐fold increase in the concentration of 5‐hydroxyindole acetic acid (5‐HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13–37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH4 administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH4 in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5‐HIAA was observed. The results suggest, the BH4 in the dosage used, is not effective in the treatment of Parkinson's disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>I. C. Dissing</name><affiliations><json:string>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</json:string></affiliations></json:item><json:item><name>F. Güttler</name><affiliations><json:string>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</json:string></affiliations></json:item><json:item><name>H. Pakkenberg</name><affiliations><json:string>Department of Neurology, Hvidovre Hospital, Denmark</json:string></affiliations></json:item><json:item><name>H. Lou</name><affiliations><json:string>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</json:string></affiliations></json:item><json:item><name>A.‐M. Gerdes</name><affiliations><json:string>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</json:string></affiliations></json:item><json:item><name>C. Lykkelund</name><affiliations><json:string>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</json:string></affiliations></json:item><json:item><name>V. Rasmussen</name><affiliations><json:string>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</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>biopterin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>dopamine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>serotonin</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HVA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>5‐HIAA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tyrosine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tryptophan</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>phenylalanine</value></json:item></subject><articleId><json:string>ANE493</json:string></articleId><language><json:string>eng</json:string></language><abstract>ABSTRACT— Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH4) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4–8 fold increase in the concentration of homovanillic acid (HVA), and a 3‐fold increase in the concentration of 5‐hydroxyindole acetic acid (5‐HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13–37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH4 administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH4 in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5‐HIAA was observed. The results suggest, the BH4 in the dosage used, is not effective in the treatment of Parkinson's disease.</abstract><qualityIndicators><score>5.398</score><pdfVersion>1.3</pdfVersion><pdfPageSize>493.2 x 709.44 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>9</keywordCount><abstractCharCount>1044</abstractCharCount><pdfWordCount>3394</pdfWordCount><pdfCharCount>22670</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>167</abstractWordCount></qualityIndicators><title>Tetrahydrobiopterin and Parkinson's disease</title><genre><json:string>article</json:string></genre><host><volume>79</volume><publisherId><json:string>ANE</json:string></publisherId><pages><total>7</total><last>499</last><first>493</first></pages><issn><json:string>0001-6314</json:string></issn><issue>6</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1600-0404</json:string></eissn><title>Acta Neurologica Scandinavica</title><doi><json:string>10.1111/(ISSN)1600-0404</json:string></doi></host><publicationDate>1989</publicationDate><copyrightDate>1989</copyrightDate><doi><json:string>10.1111/j.1600-0404.1989.tb03820.x</json:string></doi><id>7655FDDCDF51677613CAF8FD228677B80485252A</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/7655FDDCDF51677613CAF8FD228677B80485252A/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/7655FDDCDF51677613CAF8FD228677B80485252A/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/7655FDDCDF51677613CAF8FD228677B80485252A/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Tetrahydrobiopterin and Parkinson's disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><availability><p>WILEY</p></availability><date>1989</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Tetrahydrobiopterin and Parkinson's disease</title><author><persName><forename type="first">I. C.</forename><surname>Dissing</surname></persName><note type="correspondence"><p>Correspondence: Norasvej 30 DK‐2920 Charlottenlund Denmark</p></note><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation></author><author><persName><forename type="first">F.</forename><surname>Güttler</surname></persName><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation></author><author><persName><forename type="first">H.</forename><surname>Pakkenberg</surname></persName><affiliation>Department of Neurology, Hvidovre Hospital, Denmark</affiliation></author><author><persName><forename type="first">H.</forename><surname>Lou</surname></persName><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation></author><author><persName><forename type="first">A.‐M.</forename><surname>Gerdes</surname></persName><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation></author><author><persName><forename type="first">C.</forename><surname>Lykkelund</surname></persName><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation></author><author><persName><forename type="first">V.</forename><surname>Rasmussen</surname></persName><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</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>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1989-06"></date><biblScope unit="volume">79</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="493">493</biblScope><biblScope unit="page" to="499">499</biblScope></imprint></monogr><idno type="istex">7655FDDCDF51677613CAF8FD228677B80485252A</idno><idno type="DOI">10.1111/j.1600-0404.1989.tb03820.x</idno><idno type="ArticleID">ANE493</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1989</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>ABSTRACT— Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH4) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4–8 fold increase in the concentration of homovanillic acid (HVA), and a 3‐fold increase in the concentration of 5‐hydroxyindole acetic acid (5‐HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13–37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH4 administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH4 in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5‐HIAA was observed. The results suggest, the BH4 in the dosage used, is not effective in the treatment of Parkinson's disease.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Parkinson's disease</term></item><item><term>biopterin</term></item><item><term>dopamine</term></item><item><term>serotonin</term></item><item><term>HVA</term></item><item><term>5‐HIAA</term></item><item><term>tyrosine</term></item><item><term>tryptophan</term></item><item><term>phenylalanine</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1989-06">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/7655FDDCDF51677613CAF8FD228677B80485252A/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>Blackwell Publishing Ltd</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="06006"><doi origin="wiley">10.1111/ane.1989.79.issue-6</doi><numberingGroup><numbering type="journalVolume" number="79">79</numbering><numbering type="journalIssue" number="6">6</numbering></numberingGroup><coverDate startDate="1989-06">June 1989</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="0049300" status="forIssue"><doi origin="wiley">10.1111/j.1600-0404.1989.tb03820.x</doi><idGroup><id type="unit" value="ANE493"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="tocHeading1">Original articles</title></titleGroup><eventGroup><event type="firstOnline" date="2009-01-29"></event><event type="publishedOnlineFinalForm" date="2009-01-29"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.6 mode:FullText source:HeaderRef result:HeaderRef" date="2010-04-20"></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="493">493</numbering><numbering type="pageLast" number="499">499</numbering></numberingGroup><correspondenceTo><i>Inger Christine Dissing</i> Norasvej 30 DK‐2920 Charlottenlund Denmark</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ANE.ANE493.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Accepted for publication December 21, 1988</unparsedEditorialHistory><countGroup><count type="referenceTotal" number="36"></count><count type="linksCrossRef" number="8"></count></countGroup><titleGroup><title type="main">Tetrahydrobiopterin and Parkinson's disease</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1" corresponding="yes"><personName><givenNames>I. C.</givenNames><familyName>Dissing</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>F.</givenNames><familyName>Güttler</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2"><personName><givenNames>H.</givenNames><familyName>Pakkenberg</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>H.</givenNames><familyName>Lou</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a1"><personName><givenNames>A.‐M.</givenNames><familyName>Gerdes</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>C.</givenNames><familyName>Lykkelund</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>V.</givenNames><familyName>Rasmussen</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DK"><unparsedAffiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="DK"><unparsedAffiliation>Department of Neurology, Hvidovre Hospital, Denmark</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Parkinson's disease</keyword><keyword xml:id="k2">biopterin</keyword><keyword xml:id="k3">dopamine</keyword><keyword xml:id="k4">serotonin</keyword><keyword xml:id="k5">HVA</keyword><keyword xml:id="k6">5‐HIAA</keyword><keyword xml:id="k7">tyrosine</keyword><keyword xml:id="k8">tryptophan</keyword><keyword xml:id="k9">phenylalanine</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p><b>ABSTRACT— </b> Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH<sub>4</sub>) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4–8 fold increase in the concentration of homovanillic acid (HVA), and a 3‐fold increase in the concentration of 5‐hydroxyindole acetic acid (5‐HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13–37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH<sub>4</sub> administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH<sub>4</sub> in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5‐HIAA was observed. The results suggest, the BH<sub>4</sub> in the dosage used, is not effective in the treatment of Parkinson's disease.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Tetrahydrobiopterin and Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Tetrahydrobiopterin and Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">I. C.</namePart><namePart type="family">Dissing</namePart><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation><description>Correspondence: Norasvej 30 DK‐2920 Charlottenlund Denmark</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.</namePart><namePart type="family">Güttler</namePart><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Pakkenberg</namePart><affiliation>Department of Neurology, Hvidovre Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">H.</namePart><namePart type="family">Lou</namePart><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.‐M.</namePart><namePart type="family">Gerdes</namePart><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Lykkelund</namePart><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">V.</namePart><namePart type="family">Rasmussen</namePart><affiliation>John F. Kennedy Institute, Glostrup, Hvidovre Hospital, Denmark</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">1989-06</dateIssued><edition>Accepted for publication December 21, 1988</edition><copyrightDate encoding="w3cdtf">1989</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="references">36</extent></physicalDescription><abstract lang="en">ABSTRACT— Two patients with Parkinson's disease were treated with 1 g tetrahydrobiopterin (BH4) for 5 days. Clinical improvement was not observed. In the cerebrospinal fluid (CSF) a 4–8 fold increase in the concentration of homovanillic acid (HVA), and a 3‐fold increase in the concentration of 5‐hydroxyindole acetic acid (5‐HIAA) was measured. However, the concentration of HVA reached, was only approximately half as high, as that of patients treated with madopar (DOPA + benserazid). In urine, the excretion of HVA increased 13–37 fold, when the patients were treated with madopar, whereas no increase in the HVA excretion was measured after the BH4 administration. Additionally, 2 patients with Parkinson's disease were treated with 1 g BH4 in combination with 15 g tyrosine for 3 days, and 1 parkinsonian patient was treated with 15 g tyrosine daily for 7 weeks. No increase in the CSF concentrations of HVA or 5‐HIAA was observed. The results suggest, the BH4 in the dosage used, is not effective in the treatment of Parkinson's disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>Parkinson's disease</topic><topic>biopterin</topic><topic>dopamine</topic><topic>serotonin</topic><topic>HVA</topic><topic>5‐HIAA</topic><topic>tyrosine</topic><topic>tryptophan</topic><topic>phenylalanine</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>1989</date><detail type="volume"><caption>vol.</caption><number>79</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>493</start><end>499</end><total>7</total></extent></part></relatedItem><identifier type="istex">7655FDDCDF51677613CAF8FD228677B80485252A</identifier><identifier type="DOI">10.1111/j.1600-0404.1989.tb03820.x</identifier><identifier type="ArticleID">ANE493</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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