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.
English descriptors
- 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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<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>
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<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>
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<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>
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<mods version="3.6"><titleInfo lang="en"><title>Tetrahydrobiopterin and Parkinson's disease</title>
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<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>
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</role>
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<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>
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<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="references">36</extent>
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<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>
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