Serveur d'exploration autour de Joseph Jankovic

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Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: the STRIDE-PD study.

Identifieur interne : 000090 ( PubMed/Corpus ); précédent : 000089; suivant : 000091

Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: the STRIDE-PD study.

Auteurs : Fabrizio Stocchi ; Olivier Rascol ; Karl Kieburtz ; Werner Poewe ; Joseph Jankovic ; Eduardo Tolosa ; Paulo Barone ; Anthony. Lang ; C Olanow

Source :

RBID : pubmed:20582993

English descriptors

Abstract

L-dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L-dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L-dopa with entacapone, an inhibitor of catechol-O-methyltransferase, to extend its elimination half-life.

DOI: 10.1002/ana.22060
PubMed: 20582993

Links to Exploration step

pubmed:20582993

Le document en format XML

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<term>Antiparkinson Agents (administration & dosage)</term>
<term>Antiparkinson Agents (adverse effects)</term>
<term>Antiparkinson Agents (therapeutic use)</term>
<term>Carbidopa (administration & dosage)</term>
<term>Carbidopa (adverse effects)</term>
<term>Carbidopa (therapeutic use)</term>
<term>Catechol O-Methyltransferase Inhibitors</term>
<term>Catechols (administration & dosage)</term>
<term>Catechols (adverse effects)</term>
<term>Catechols (therapeutic use)</term>
<term>Disease Progression</term>
<term>Dopamine Agents (administration & dosage)</term>
<term>Dopamine Agents (adverse effects)</term>
<term>Dopamine Agents (therapeutic use)</term>
<term>Double-Blind Method</term>
<term>Drug Therapy, Combination</term>
<term>Dyskinesia, Drug-Induced (epidemiology)</term>
<term>Enzyme Inhibitors (administration & dosage)</term>
<term>Enzyme Inhibitors (adverse effects)</term>
<term>Enzyme Inhibitors (therapeutic use)</term>
<term>Female</term>
<term>Humans</term>
<term>Levodopa (administration & dosage)</term>
<term>Levodopa (adverse effects)</term>
<term>Levodopa (therapeutic use)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Nitriles (administration & dosage)</term>
<term>Nitriles (adverse effects)</term>
<term>Nitriles (therapeutic use)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (epidemiology)</term>
<term>Risk</term>
<term>Time Factors</term>
<term>Treatment Outcome</term>
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<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en">
<term>Antiparkinson Agents</term>
<term>Carbidopa</term>
<term>Catechols</term>
<term>Dopamine Agents</term>
<term>Enzyme Inhibitors</term>
<term>Levodopa</term>
<term>Nitriles</term>
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<term>Antiparkinson Agents</term>
<term>Carbidopa</term>
<term>Catechols</term>
<term>Dopamine Agents</term>
<term>Enzyme Inhibitors</term>
<term>Levodopa</term>
<term>Nitriles</term>
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<term>Antiparkinson Agents</term>
<term>Carbidopa</term>
<term>Catechols</term>
<term>Dopamine Agents</term>
<term>Enzyme Inhibitors</term>
<term>Levodopa</term>
<term>Nitriles</term>
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<term>Catechol O-Methyltransferase Inhibitors</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en">
<term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en">
<term>Dyskinesia, Drug-Induced</term>
<term>Parkinson Disease</term>
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<term>Double-Blind Method</term>
<term>Drug Therapy, Combination</term>
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<term>Humans</term>
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<front>
<div type="abstract" xml:lang="en">L-dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L-dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L-dopa with entacapone, an inhibitor of catechol-O-methyltransferase, to extend its elimination half-life.</div>
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<DateCreated>
<Year>2010</Year>
<Month>07</Month>
<Day>01</Day>
</DateCreated>
<DateCompleted>
<Year>2010</Year>
<Month>07</Month>
<Day>20</Day>
</DateCompleted>
<DateRevised>
<Year>2014</Year>
<Month>11</Month>
<Day>20</Day>
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<ISSN IssnType="Electronic">1531-8249</ISSN>
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<Volume>68</Volume>
<Issue>1</Issue>
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<Year>2010</Year>
<Month>Jul</Month>
</PubDate>
</JournalIssue>
<Title>Annals of neurology</Title>
<ISOAbbreviation>Ann. Neurol.</ISOAbbreviation>
</Journal>
<ArticleTitle>Initiating levodopa/carbidopa therapy with and without entacapone in early Parkinson disease: the STRIDE-PD study.</ArticleTitle>
<Pagination>
<MedlinePgn>18-27</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1002/ana.22060</ELocationID>
<Abstract>
<AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">L-dopa is the most widely used and most effective therapy for Parkinson disease (PD), but chronic treatment is associated with motor complications in the majority of patients. It has been hypothesized that providing more continuous delivery of L-dopa to the brain would reduce the risk of motor complications, and that this might be accomplished by combining L-dopa with entacapone, an inhibitor of catechol-O-methyltransferase, to extend its elimination half-life.</AbstractText>
<AbstractText Label="METHODS" NlmCategory="METHODS">We performed a prospective 134-week double-blind trial comparing the risk of developing dyskinesia in 747 PD patients randomized to initiate L-dopa therapy with L-dopa/carbidopa (LC) or L-dopa/carbidopa/entacapone (LCE), administered 4x daily at 3.5-hour intervals. The primary endpoint was time to onset of dyskinesia.</AbstractText>
<AbstractText Label="RESULTS" NlmCategory="RESULTS">In comparison to LC, patients receiving LCE had a shorter time to onset of dyskinesia (hazard ratio, 1.29; p = 0.04) and increased frequency at week 134 (42% vs 32%; p = 0.02). These effects were more pronounced in patients receiving dopamine agonists at baseline. Time to wearing off and motor scores were not significantly different, but trended in favor of LCE treatment. Patients in the LCE group received greater L-dopa dose equivalents than LC-treated patients (p < 0.001).</AbstractText>
<AbstractText Label="INTERPRETATION" NlmCategory="CONCLUSIONS">Initiating L-dopa therapy with LCE failed to delay the time of onset or reduce the frequency of dyskinesia compared to LC. In fact, LCE was associated with a shorter time to onset and increased frequency of dyskinesia compared to LC. These results may reflect that the treatment protocol employed did not provide continuous L-dopa availability and the higher L-dopa dose equivalents in the LCE group.</AbstractText>
</Abstract>
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<LastName>Stocchi</LastName>
<ForeName>Fabrizio</ForeName>
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<Affiliation>Institute of Neurology, IRCCS San Raffaele Pisana, Rome, Italy.</Affiliation>
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<Chemical>
<RegistryNumber>4975G9NM6T</RegistryNumber>
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<CommentsCorrections RefType="CommentIn">
<RefSource>Ann Neurol. 2010 Jul;68(1):3-5</RefSource>
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</CommentsCorrections>
<CommentsCorrections RefType="CommentIn">
<RefSource>J Neurol. 2010 Sep;257(9):1587-9</RefSource>
<PMID Version="1">20706844</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="CommentIn">
<RefSource>Ann Neurol. 2011 Feb;69(2):424; author reply 425</RefSource>
<PMID Version="1">21387388</PMID>
</CommentsCorrections>
<CommentsCorrections RefType="ErratumIn">
<RefSource>Ann Neurol. 2010 Sep;68(3):412-3</RefSource>
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<DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName>
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<MeshHeading>
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