La maladie de Parkinson au Canada (serveur d'exploration)

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Rivastigmine for dementia associated with Parkinson's disease

Identifieur interne : 000379 ( PascalFrancis/Curation ); précédent : 000378; suivant : 000380

Rivastigmine for dementia associated with Parkinson's disease

Auteurs : Murat Emre [Turquie] ; Dag Aarsland [Norvège] ; Albeao Albanese [Italie] ; E. Jane Byrne [Royaume-Uni] ; Günther Deuschl [Allemagne] ; Peter P. De Deyn [Belgique] ; Franck Durif [France] ; Jaime Kulisevsky [Espagne] ; Teus Van Laar [Pays-Bas] ; Andrew Lees [Royaume-Uni] ; Werner Poewe [Autriche] ; Alain Robillard [Canada] ; Mario M. Rosa [Portugal] ; Erik Wolters [Pays-Bas] ; Peter Quarg [Suisse] ; Sibel Tekin [États-Unis] ; Roger Lane [États-Unis]

Source :

RBID : Pascal:05-0025297

Descripteurs français

English descriptors

Abstract

BACKGROUND Cholinergic deficits are prominent in patients who have dementia associated with Parkinson's disease. We investigated the effects of the dual cholinesterase inhibitor rivastigmine in such patients. METHODS Patients in whom mild-to-moderate dementia developed at least 2 years after they received a clinical diagnosis of Parkinson's disease were randomly assigned to receive placebo or 3 to 12 mg of rivastigmine per day for 24 weeks. Primary efficacy variables were the scores for the cognitive subscale ofthe Alzheimer's Disease Assessment Scale (ADAS-cog) and Alzheimer's Disease Cooperative Study-Clinician's Global Impression of Change (ADCS-CGIC). Secondary clinical outcomes were the scores for the Alzheimer's Disease Cooperative Study-Activities of Daily Living, the 10-item Neuropsychiatric Inventory, the Mini-Mental State Examination, Cognitive Drug Research power of attention tests, the Verbal Fluency test, and the Ten Point Clock-Drawing test. RESULTS A total of 541 patients were enrolled, and 410 completed the study. The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. Rivastigmine-treated patients had a mean improvement of2.1 points in the score for the 70-point ADAS-cog, from a baseline score of 23.8, as compared with a 0.7-point worsening in the placebo group, from a baseline score of 24.3 (P<0.001). Clinically meaningful improvements in the scores for the ADCS-CGIC were observed in 19.8 percent of patients in the rivastigmine group and 14.5 percent ofthose in the placebo group, and clinically meaningful worsening was observed in 13.0 percent and 23.1 percent, respectively (mean score at 24 weeks, 3.8 and 4.3, respectively; P=0.007). Significantly better outcomes were seen with rivastigmine with respect to all secondary efficacy variables. The most frequent adverse events were nausea (affecting 29.0 percent of patients in the rivastigmine group and 11.2 percent of those in the placebo group, P<0.001), vomiting (16.6 and 1.7 percent, P<0.001), and tremor (10.2 and 3.9 percent, P=:0.01). CONCLUSIONS In this placebo-controlled study, rivastigmine was associated with moderate improvements in dementia associated with Parkinson's disease but also with higher rates of nausea, vomiting, and tremor.
pA  
A01 01  1    @0 0028-4793
A02 01      @0 NEJMAG
A03   1    @0 N. Engl. j. med.
A05       @2 351
A06       @2 24
A08 01  1  ENG  @1 Rivastigmine for dementia associated with Parkinson's disease
A11 01  1    @1 EMRE (Murat)
A11 02  1    @1 AARSLAND (Dag)
A11 03  1    @1 ALBANESE (Albeao)
A11 04  1    @1 BYRNE (E. Jane)
A11 05  1    @1 DEUSCHL (Günther)
A11 06  1    @1 DE DEYN (Peter P.)
A11 07  1    @1 DURIF (Franck)
A11 08  1    @1 KULISEVSKY (Jaime)
A11 09  1    @1 VAN LAAR (Teus)
A11 10  1    @1 LEES (Andrew)
A11 11  1    @1 POEWE (Werner)
A11 12  1    @1 ROBILLARD (Alain)
A11 13  1    @1 ROSA (Mario M.)
A11 14  1    @1 WOLTERS (Erik)
A11 15  1    @1 QUARG (Peter)
A11 16  1    @1 TEKIN (Sibel)
A11 17  1    @1 LANE (Roger)
A14 01      @1 Istanbul Faculty of Medicine, Istanbul University @2 Istanbul @3 TUR @Z 1 aut.
A14 02      @1 Rogaland Central Hospital @2 Stavanger @3 NOR @Z 2 aut.
A14 03      @1 School of Medicine, University of Bergen @2 Bergen @3 NOR @Z 2 aut.
A14 04      @1 Istituto Nazionale Neurologico Carlo Besta and Università Cattolica @2 Milan @3 ITA @Z 3 aut.
A14 05      @1 University of Manchester @2 Manchester @3 GBR @Z 4 aut.
A14 06      @1 Christian-Albrechts-Universität Kiel @2 Kiel @3 DEU @Z 5 aut.
A14 07      @1 Middelheim Hospital, Zeikenhuis Netwerk Antwerpen, and the Born-Bunge Foundation, University of Antwerp @2 Wilrijk-Antwerp @3 BEL @Z 6 aut.
A14 08      @1 Centre Hospitalier Universitaire Clermont-Ferrand @2 Clermont-Ferrand @3 FRA @Z 7 aut.
A14 09      @1 Sant Pau Hospital @2 Barcelona @3 ESP @Z 8 aut.
A14 10      @1 Groningen University Hospital @2 Groningen @3 NLD @Z 9 aut.
A14 11      @1 Reta Lila Weston Institute for Neurological Studies, University College London @2 London @3 GBR @Z 10 aut.
A14 12      @1 Innsbruck Medical University @2 Innsbruck @3 AUT @Z 11 aut.
A14 13      @1 Hôpital Maisonneuve-Rosemont @2 Montreal @3 CAN @Z 12 aut.
A14 14      @1 Hospital de Santa Maria @2 Lisbon @3 PRT @Z 13 aut.
A14 15      @1 Research Institute for Neurosciences, Vrije Universiteit Medical Center @2 Amsterdam @3 NLD @Z 14 aut.
A14 16      @1 Novartis Pharma @2 Basel @3 CHE @Z 15 aut.
A14 17      @1 Novartis Pharmaceuticals @2 East Hanover, N.J. @3 USA @Z 16 aut. @Z 17 aut.
A20       @1 2509-2518
A21       @1 2004
A23 01      @0 ENG
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A60       @1 P
A61       @0 A
A64 01  1    @0 The New England journal of medicine
A66 01      @0 USA
C01 01    ENG  @0 BACKGROUND Cholinergic deficits are prominent in patients who have dementia associated with Parkinson's disease. We investigated the effects of the dual cholinesterase inhibitor rivastigmine in such patients. METHODS Patients in whom mild-to-moderate dementia developed at least 2 years after they received a clinical diagnosis of Parkinson's disease were randomly assigned to receive placebo or 3 to 12 mg of rivastigmine per day for 24 weeks. Primary efficacy variables were the scores for the cognitive subscale ofthe Alzheimer's Disease Assessment Scale (ADAS-cog) and Alzheimer's Disease Cooperative Study-Clinician's Global Impression of Change (ADCS-CGIC). Secondary clinical outcomes were the scores for the Alzheimer's Disease Cooperative Study-Activities of Daily Living, the 10-item Neuropsychiatric Inventory, the Mini-Mental State Examination, Cognitive Drug Research power of attention tests, the Verbal Fluency test, and the Ten Point Clock-Drawing test. RESULTS A total of 541 patients were enrolled, and 410 completed the study. The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. Rivastigmine-treated patients had a mean improvement of2.1 points in the score for the 70-point ADAS-cog, from a baseline score of 23.8, as compared with a 0.7-point worsening in the placebo group, from a baseline score of 24.3 (P<0.001). Clinically meaningful improvements in the scores for the ADCS-CGIC were observed in 19.8 percent of patients in the rivastigmine group and 14.5 percent ofthose in the placebo group, and clinically meaningful worsening was observed in 13.0 percent and 23.1 percent, respectively (mean score at 24 weeks, 3.8 and 4.3, respectively; P=0.007). Significantly better outcomes were seen with rivastigmine with respect to all secondary efficacy variables. The most frequent adverse events were nausea (affecting 29.0 percent of patients in the rivastigmine group and 11.2 percent of those in the placebo group, P<0.001), vomiting (16.6 and 1.7 percent, P<0.001), and tremor (10.2 and 3.9 percent, P=:0.01). CONCLUSIONS In this placebo-controlled study, rivastigmine was associated with moderate improvements in dementia associated with Parkinson's disease but also with higher rates of nausea, vomiting, and tremor.
C02 01  X    @0 002B01
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C07 06  X  FRE  @0 Anticholinestérasique @5 38
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C07 12  X  SPA  @0 Sistema nervioso patología @5 45
N21       @1 010
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Pascal:05-0025297

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<title xml:lang="en" level="a">Rivastigmine for dementia associated with Parkinson's disease</title>
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<name sortKey="Albanese, Albeao" sort="Albanese, Albeao" uniqKey="Albanese A" first="Albeao" last="Albanese">Albeao Albanese</name>
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<name sortKey="Byrne, E Jane" sort="Byrne, E Jane" uniqKey="Byrne E" first="E. Jane" last="Byrne">E. Jane Byrne</name>
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<title level="j" type="main">The New England journal of medicine</title>
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<div type="abstract" xml:lang="en">BACKGROUND Cholinergic deficits are prominent in patients who have dementia associated with Parkinson's disease. We investigated the effects of the dual cholinesterase inhibitor rivastigmine in such patients. METHODS Patients in whom mild-to-moderate dementia developed at least 2 years after they received a clinical diagnosis of Parkinson's disease were randomly assigned to receive placebo or 3 to 12 mg of rivastigmine per day for 24 weeks. Primary efficacy variables were the scores for the cognitive subscale ofthe Alzheimer's Disease Assessment Scale (ADAS-cog) and Alzheimer's Disease Cooperative Study-Clinician's Global Impression of Change (ADCS-CGIC). Secondary clinical outcomes were the scores for the Alzheimer's Disease Cooperative Study-Activities of Daily Living, the 10-item Neuropsychiatric Inventory, the Mini-Mental State Examination, Cognitive Drug Research power of attention tests, the Verbal Fluency test, and the Ten Point Clock-Drawing test. RESULTS A total of 541 patients were enrolled, and 410 completed the study. The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. Rivastigmine-treated patients had a mean improvement of2.1 points in the score for the 70-point ADAS-cog, from a baseline score of 23.8, as compared with a 0.7-point worsening in the placebo group, from a baseline score of 24.3 (P<0.001). Clinically meaningful improvements in the scores for the ADCS-CGIC were observed in 19.8 percent of patients in the rivastigmine group and 14.5 percent ofthose in the placebo group, and clinically meaningful worsening was observed in 13.0 percent and 23.1 percent, respectively (mean score at 24 weeks, 3.8 and 4.3, respectively; P=0.007). Significantly better outcomes were seen with rivastigmine with respect to all secondary efficacy variables. The most frequent adverse events were nausea (affecting 29.0 percent of patients in the rivastigmine group and 11.2 percent of those in the placebo group, P<0.001), vomiting (16.6 and 1.7 percent, P<0.001), and tremor (10.2 and 3.9 percent, P=:0.01). CONCLUSIONS In this placebo-controlled study, rivastigmine was associated with moderate improvements in dementia associated with Parkinson's disease but also with higher rates of nausea, vomiting, and tremor.</div>
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<s0>BACKGROUND Cholinergic deficits are prominent in patients who have dementia associated with Parkinson's disease. We investigated the effects of the dual cholinesterase inhibitor rivastigmine in such patients. METHODS Patients in whom mild-to-moderate dementia developed at least 2 years after they received a clinical diagnosis of Parkinson's disease were randomly assigned to receive placebo or 3 to 12 mg of rivastigmine per day for 24 weeks. Primary efficacy variables were the scores for the cognitive subscale ofthe Alzheimer's Disease Assessment Scale (ADAS-cog) and Alzheimer's Disease Cooperative Study-Clinician's Global Impression of Change (ADCS-CGIC). Secondary clinical outcomes were the scores for the Alzheimer's Disease Cooperative Study-Activities of Daily Living, the 10-item Neuropsychiatric Inventory, the Mini-Mental State Examination, Cognitive Drug Research power of attention tests, the Verbal Fluency test, and the Ten Point Clock-Drawing test. RESULTS A total of 541 patients were enrolled, and 410 completed the study. The outcomes were better among patients treated with rivastigmine than among those who received placebo; however, the differences between these two groups were moderate and similar to those reported in trials of rivastigmine for Alzheimer's disease. Rivastigmine-treated patients had a mean improvement of2.1 points in the score for the 70-point ADAS-cog, from a baseline score of 23.8, as compared with a 0.7-point worsening in the placebo group, from a baseline score of 24.3 (P<0.001). Clinically meaningful improvements in the scores for the ADCS-CGIC were observed in 19.8 percent of patients in the rivastigmine group and 14.5 percent ofthose in the placebo group, and clinically meaningful worsening was observed in 13.0 percent and 23.1 percent, respectively (mean score at 24 weeks, 3.8 and 4.3, respectively; P=0.007). Significantly better outcomes were seen with rivastigmine with respect to all secondary efficacy variables. The most frequent adverse events were nausea (affecting 29.0 percent of patients in the rivastigmine group and 11.2 percent of those in the placebo group, P<0.001), vomiting (16.6 and 1.7 percent, P<0.001), and tremor (10.2 and 3.9 percent, P=:0.01). CONCLUSIONS In this placebo-controlled study, rivastigmine was associated with moderate improvements in dementia associated with Parkinson's disease but also with higher rates of nausea, vomiting, and tremor.</s0>
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<fC07 i1="02" i2="X" l="FRE">
<s0>Carboxylic ester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Carboxylic ester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Carboxylic ester hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Esterases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Hydrolases</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Enzyme</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Enzima</s0>
<s2>FE</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Anticholinestérasique</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Anticholinesterase agent</s0>
<s5>38</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Anticolinesterasa agente</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Inhibiteur enzyme</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Enzyme inhibitor</s0>
<s5>39</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Inhibidor enzima</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Encéphale pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>40</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>41</s5>
</fC07>
<fC07 i1="10" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>42</s5>
</fC07>
<fC07 i1="10" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>42</s5>
</fC07>
<fC07 i1="11" i2="X" l="FRE">
<s0>Système nerveux central pathologie</s0>
<s5>43</s5>
</fC07>
<fC07 i1="11" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>43</s5>
</fC07>
<fC07 i1="11" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>43</s5>
</fC07>
<fC07 i1="12" i2="X" l="FRE">
<s0>Système nerveux pathologie</s0>
<s5>45</s5>
</fC07>
<fC07 i1="12" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>45</s5>
</fC07>
<fC07 i1="12" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>45</s5>
</fC07>
<fN21>
<s1>010</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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