ParkinsonCanadaV1, PascalFrancis, Corpus, bibRecord, 000420

Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study

Identifieur interne : 000420 ( PascalFrancis/Corpus ); précédent : 000419; suivant : 000421

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 E. Lang ; C. Warren Olanow

Source :

Annals of neurology [ 0364-5134 ] ; 2010.

RBID : Pascal:10-0343678

Descripteurs français

Pascal (Inist)
- Maladie de Parkinson, Pathologie du système nerveux, Lévodopa, Carbidopa, Traitement, Entacapone.

English descriptors

KwdEn :
- Carbidopa, Entacapone, Levodopa, Nervous system diseases, Parkinson disease, Treatment.

Abstract

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. 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. 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). Interpretation: 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.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

A01	`01`	`1`		`@0 0364-5134`
A02	`01`			`@0 ANNED3`
A03		`1`		`@0 Ann. neurol.`
A05				`@2 68`
A06				`@2 1`
A08	`01`	`1`	`ENG`	`@1 Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study`
A11	`01`	`1`		`@1 STOCCHI (Fabrizio)`
A11	`02`	`1`		`@1 RASCOL (Olivier)`
A11	`03`	`1`		`@1 KIEBURTZ (Karl)`
A11	`04`	`1`		`@1 POEWE (Werner)`
A11	`05`	`1`		`@1 JANKOVIC (Joseph)`
A11	`06`	`1`		`@1 TOLOSA (Eduardo)`
A11	`07`	`1`		`@1 BARONE (Paulo)`
A11	`08`	`1`		`@1 LANG (Anthony E.)`
A11	`09`	`1`		`@1 WARREN OLANOW (C.)`
A14	`01`			`@1 Institute of Neurology, IRCCS San Raffaele Pisana @2 Rome @3 ITA @Z 1 aut.`
A14	`02`			`@1 INSERM U455, Clinical Investigation Center @3 FRA @Z 2 aut.`
A14	`03`			`@1 Department of Clinical Pharmacology, Faculty of Medicine @2 Toulouse @3 FRA @Z 2 aut.`
A14	`04`			`@1 Department of Neurosciences, Faculty of Medicine @2 Toulouse @3 FRA @Z 2 aut.`
A14	`05`			`@1 Department of Neurology, University of Rochester @2 Rochester, NY @3 USA @Z 3 aut.`
A14	`06`			`@1 Department of Neurology, Innsbruck Medical University @2 Innsbruck @3 AUT @Z 4 aut.`
A14	`07`			`@1 Department of Neurology, Baylor College of Medicine @2 Houston, TX @3 USA @Z 5 aut.`
A14	`08`			`@1 Neurology Service, Hospital Clinic, University of Barcelona @2 Barcelona @3 ESP @Z 6 aut.`
A14	`09`			`@1 Department of Neurological Sciences, University of Naples and IDC-Hermitage @2 Naples @3 ITA @Z 7 aut.`
A14	`10`			`@1 Division of Neurology, University of Toronto @2 Toronto @3 CAN @Z 8 aut.`
A14	`11`			`@1 Department of Neurology and Neuroscience, Mount Sinai School of Medicine @2 New York, NY @3 USA @Z 9 aut.`
A20				`@1 18-27`
A21				`@1 2010`
A23	`01`			`@0 ENG`
A43	`01`			`@1 INIST @2 16555 @5 354000193760040060`
A44				`@0 0000 @1 © 2010 INIST-CNRS. All rights reserved.`
A45				`@0 33 ref.`
A47	`01`	`1`		`@0 10-0343678`
A60				`@1 P`
A61				`@0 A`
A64	`01`	`1`		`@0 Annals of neurology`
A66	`01`			`@0 USA`
C01	`01`		`ENG`	@0 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. 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. 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). Interpretation: 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.
C02	`01`	`X`		`@0 002B17`
C02	`02`	`X`		`@0 002B17G`
C03	`01`	`X`	`FRE`	`@0 Maladie de Parkinson @2 NM @5 01`
C03	`01`	`X`	`ENG`	`@0 Parkinson disease @2 NM @5 01`
C03	`01`	`X`	`SPA`	`@0 Parkinson enfermedad @2 NM @5 01`
C03	`02`	`X`	`FRE`	`@0 Pathologie du système nerveux @5 02`
C03	`02`	`X`	`ENG`	`@0 Nervous system diseases @5 02`
C03	`02`	`X`	`SPA`	`@0 Sistema nervioso patología @5 02`
C03	`03`	`X`	`FRE`	`@0 Lévodopa @2 NK @2 FR @5 09`
C03	`03`	`X`	`ENG`	`@0 Levodopa @2 NK @2 FR @5 09`
C03	`03`	`X`	`SPA`	`@0 Levodopa @2 NK @2 FR @5 09`
C03	`04`	`X`	`FRE`	`@0 Carbidopa @2 NK @2 FR @5 10`
C03	`04`	`X`	`ENG`	`@0 Carbidopa @2 NK @2 FR @5 10`
C03	`04`	`X`	`SPA`	`@0 Carbidopa @2 NK @2 FR @5 10`
C03	`05`	`X`	`FRE`	`@0 Traitement @5 11`
C03	`05`	`X`	`ENG`	`@0 Treatment @5 11`
C03	`05`	`X`	`SPA`	`@0 Tratamiento @5 11`
C03	`06`	`X`	`FRE`	`@0 Entacapone @2 NK @2 FR @5 12`
C03	`06`	`X`	`ENG`	`@0 Entacapone @2 NK @2 FR @5 12`
C03	`06`	`X`	`SPA`	`@0 Entacapona @2 NK @2 FR @5 12`
C07	`01`	`X`	`FRE`	`@0 Pathologie de l'encéphale @5 37`
C07	`01`	`X`	`ENG`	`@0 Cerebral disorder @5 37`
C07	`01`	`X`	`SPA`	`@0 Encéfalo patología @5 37`
C07	`02`	`X`	`FRE`	`@0 Syndrome extrapyramidal @5 38`
C07	`02`	`X`	`ENG`	`@0 Extrapyramidal syndrome @5 38`
C07	`02`	`X`	`SPA`	`@0 Extrapiramidal síndrome @5 38`
C07	`03`	`X`	`FRE`	`@0 Maladie dégénérative @5 39`
C07	`03`	`X`	`ENG`	`@0 Degenerative disease @5 39`
C07	`03`	`X`	`SPA`	`@0 Enfermedad degenerativa @5 39`
C07	`04`	`X`	`FRE`	`@0 Pathologie du système nerveux central @5 40`
C07	`04`	`X`	`ENG`	`@0 Central nervous system disease @5 40`
C07	`04`	`X`	`SPA`	`@0 Sistema nervosio central patología @5 40`
N21				`@1 221`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 10-0343678 INIST
ET :	Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study
AU :	STOCCHI (Fabrizio); RASCOL (Olivier); KIEBURTZ (Karl); POEWE (Werner); JANKOVIC (Joseph); TOLOSA (Eduardo); BARONE (Paulo); LANG (Anthony E.); WARREN OLANOW (C.)
AF :	Institute of Neurology, IRCCS San Raffaele Pisana/Rome/Italie (1 aut.); INSERM U455, Clinical Investigation Center/France (2 aut.); Department of Clinical Pharmacology, Faculty of Medicine/Toulouse/France (2 aut.); Department of Neurosciences, Faculty of Medicine/Toulouse/France (2 aut.); Department of Neurology, University of Rochester/Rochester, NY/Etats-Unis (3 aut.); Department of Neurology, Innsbruck Medical University/Innsbruck/Autriche (4 aut.); Department of Neurology, Baylor College of Medicine/Houston, TX/Etats-Unis (5 aut.); Neurology Service, Hospital Clinic, University of Barcelona/Barcelona/Espagne (6 aut.); Department of Neurological Sciences, University of Naples and IDC-Hermitage/Naples/Italie (7 aut.); Division of Neurology, University of Toronto/Toronto/Canada (8 aut.); Department of Neurology and Neuroscience, Mount Sinai School of Medicine/New York, NY/Etats-Unis (9 aut.)
DT :	Publication en série; Niveau analytique
SO :	Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2010; Vol. 68; No. 1; Pp. 18-27; Bibl. 33 ref.
LA :	Anglais
EA :	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. 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. 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). Interpretation: 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.
CC :	002B17; 002B17G
FD :	Maladie de Parkinson; Pathologie du système nerveux; Lévodopa; Carbidopa; Traitement; Entacapone
FG :	Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du système nerveux central
ED :	Parkinson disease; Nervous system diseases; Levodopa; Carbidopa; Treatment; Entacapone
EG :	Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease
SD :	Parkinson enfermedad; Sistema nervioso patología; Levodopa; Carbidopa; Tratamiento; Entacapona
LO :	INIST-16555.354000193760040060
ID :	10-0343678

Links to Exploration step

Pascal:10-0343678

Le document en format XML

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<front><div type="abstract" xml:lang="en">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. 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. 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). Interpretation: 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.</div>
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<fA03 i2="1"><s0>Ann. neurol.</s0>
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<fA05><s2>68</s2>
</fA05>
<fA06><s2>1</s2>
</fA06>
<fA08 i1="01" i2="1" l="ENG"><s1>Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study</s1>
</fA08>
<fA11 i1="01" i2="1"><s1>STOCCHI (Fabrizio)</s1>
</fA11>
<fA11 i1="02" i2="1"><s1>RASCOL (Olivier)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>KIEBURTZ (Karl)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>POEWE (Werner)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>JANKOVIC (Joseph)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>TOLOSA (Eduardo)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>BARONE (Paulo)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>LANG (Anthony E.)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>WARREN OLANOW (C.)</s1>
</fA11>
<fA14 i1="01"><s1>Institute of Neurology, IRCCS San Raffaele Pisana</s1>
<s2>Rome</s2>
<s3>ITA</s3>
<sZ>1 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>INSERM U455, Clinical Investigation Center</s1>
<s3>FRA</s3>
<sZ>2 aut.</sZ>
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<fA14 i1="03"><s1>Department of Clinical Pharmacology, Faculty of Medicine</s1>
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<s3>FRA</s3>
<sZ>2 aut.</sZ>
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<s3>FRA</s3>
<sZ>2 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Department of Neurology, University of Rochester</s1>
<s2>Rochester, NY</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
</fA14>
<fA14 i1="06"><s1>Department of Neurology, Innsbruck Medical University</s1>
<s2>Innsbruck</s2>
<s3>AUT</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="07"><s1>Department of Neurology, Baylor College of Medicine</s1>
<s2>Houston, TX</s2>
<s3>USA</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="08"><s1>Neurology Service, Hospital Clinic, University of Barcelona</s1>
<s2>Barcelona</s2>
<s3>ESP</s3>
<sZ>6 aut.</sZ>
</fA14>
<fA14 i1="09"><s1>Department of Neurological Sciences, University of Naples and IDC-Hermitage</s1>
<s2>Naples</s2>
<s3>ITA</s3>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="10"><s1>Division of Neurology, University of Toronto</s1>
<s2>Toronto</s2>
<s3>CAN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="11"><s1>Department of Neurology and Neuroscience, Mount Sinai School of Medicine</s1>
<s2>New York, NY</s2>
<s3>USA</s3>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>18-27</s1>
</fA20>
<fA21><s1>2010</s1>
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<fA61><s0>A</s0>
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<fA66 i1="01"><s0>USA</s0>
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<fC01 i1="01" l="ENG"><s0>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. 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. 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). Interpretation: 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.</s0>
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<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Maladie de Parkinson</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s2>NM</s2>
<s5>01</s5>
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<s5>01</s5>
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<s5>02</s5>
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</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>02</s5>
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<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Levodopa</s0>
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<s2>FR</s2>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Levodopa</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>09</s5>
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<fC03 i1="04" i2="X" l="FRE"><s0>Carbidopa</s0>
<s2>NK</s2>
<s2>FR</s2>
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<s2>FR</s2>
<s5>10</s5>
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<fC03 i1="04" i2="X" l="SPA"><s0>Carbidopa</s0>
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<s2>FR</s2>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Traitement</s0>
<s5>11</s5>
</fC03>
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<s5>11</s5>
</fC03>
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<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Entacapone</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>12</s5>
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<fC03 i1="06" i2="X" l="ENG"><s0>Entacapone</s0>
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<s2>FR</s2>
<s5>12</s5>
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<s2>NK</s2>
<s2>FR</s2>
<s5>12</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
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<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Maladie dégénérative</s0>
<s5>39</s5>
</fC07>
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<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie du   système nerveux central</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Central nervous system disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0>
<s5>40</s5>
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<fN21><s1>221</s1>
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<fN44 i1="01"><s1>OTO</s1>
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<server><NO>PASCAL 10-0343678 INIST</NO>
<ET>Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study</ET>
<AU>STOCCHI (Fabrizio); RASCOL (Olivier); KIEBURTZ (Karl); POEWE (Werner); JANKOVIC (Joseph); TOLOSA (Eduardo); BARONE (Paulo); LANG (Anthony E.); WARREN OLANOW (C.)</AU>
<AF>Institute of Neurology, IRCCS San Raffaele Pisana/Rome/Italie (1 aut.); INSERM U455, Clinical Investigation Center/France (2 aut.); Department of Clinical Pharmacology, Faculty of Medicine/Toulouse/France (2 aut.); Department of Neurosciences, Faculty of Medicine/Toulouse/France (2 aut.); Department of Neurology, University of Rochester/Rochester, NY/Etats-Unis (3 aut.); Department of Neurology, Innsbruck Medical University/Innsbruck/Autriche (4 aut.); Department of Neurology, Baylor College of Medicine/Houston, TX/Etats-Unis (5 aut.); Neurology Service, Hospital Clinic, University of Barcelona/Barcelona/Espagne (6 aut.); Department of Neurological Sciences, University of Naples and IDC-Hermitage/Naples/Italie (7 aut.); Division of Neurology, University of Toronto/Toronto/Canada (8 aut.); Department of Neurology and Neuroscience, Mount Sinai School of Medicine/New York, NY/Etats-Unis (9 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Annals of neurology; ISSN 0364-5134; Coden ANNED3; Etats-Unis; Da. 2010; Vol. 68; No. 1; Pp. 18-27; Bibl. 33 ref.</SO>
<LA>Anglais</LA>
<EA>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. 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. 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). Interpretation: 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.</EA>
<CC>002B17; 002B17G</CC>
<FD>Maladie de Parkinson; Pathologie du   système nerveux; Lévodopa; Carbidopa; Traitement; Entacapone</FD>
<FG>Pathologie de l'encéphale; Syndrome extrapyramidal; Maladie dégénérative; Pathologie du   système nerveux central</FG>
<ED>Parkinson disease; Nervous system diseases; Levodopa; Carbidopa; Treatment; Entacapone</ED>
<EG>Cerebral disorder; Extrapyramidal syndrome; Degenerative disease; Central nervous system disease</EG>
<SD>Parkinson enfermedad; Sistema nervioso patología; Levodopa; Carbidopa; Tratamiento; Entacapona</SD>
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	La maladie de Parkinson au Canada (serveur d'exploration)
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La maladie de Parkinson au Canada (serveur d'exploration)

Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study

Initiating Levodopa/Carbidopa Therapy With and Without Entacapone in Early Parkinson Disease: The STRIDE-PD Study

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