Serum Urate as a Predictor of Clinical and Radiographic Progression in Parkinson Disease. Commentary
Identifieur interne : 002381 ( Main/Curation ); précédent : 002380; suivant : 002382Serum Urate as a Predictor of Clinical and Radiographic Progression in Parkinson Disease. Commentary
Auteurs : Mya Schiess [États-Unis] ; Irene Oh ; Michael A. Schwarzschild [États-Unis] ; Steven R. Schwid [États-Unis] ; Kenneth Marek [États-Unis] ; Arthur Watts [États-Unis] ; Anthony E. Lang [Canada] ; David Oakes [États-Unis] ; Ira Shoulson [États-Unis] ; Alberto Ascherio [États-Unis]Source :
- Archives of neurology : (Chicago) [ 0003-9942 ] ; 2008.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Objective: To determine whether concentration of serum urate, a purine metabolite and potent antioxidant that has been linked to a reduced risk of Parkinson disease (PD), predicts prognosis in PD. Design: Prospective study. Setting: The Parkinson Research Examination of CEP-1347 Trial (PRECEPT) study, which investigated the effects of a potential neuroprotectant on rates of PD progression, was conducted between April 2002 and August 2005 (average follow-up time 21.4 months). Participants: Eight hundred four subjects with early PD enrolled in the PRECEPT study. Main Outcome Measures: The primary study end point was progression to clinical disability sufficient to warrant dopaminergic therapy. Cox proportional hazards models were used to estimate the hazard ratio (HR) of reaching end point according to quintiles of baseline serum urate concentration, adjusting for sex, age, and other potential covariates. Change in striatal uptake of iodine I 123-labeled 2-beta-carbomethoxy-3-beta-(4-iodophenyl) tropane ([123I] β-CIT), a marker for the presynaptic dopamine transporter, was assessed with linear regression for a subset of 399 subjects. Results: The adjusted HR of reaching end point declined with increasing baseline concentrations of urate; subjects in the top quintile reached the end point at only half the rate of subjects in the bottom quintile (HR, 0.51; 95% confidence interval [CI], 0.37-0.72; P for trend<.001). This association was markedly stronger in men (HR, 0.39; 95% CI, 0.26-0.60; P for trend <.001) than in women (HR, 0.77; 95% CI, 0.39-1.50; P for trend=.33). The percentage of loss in striatal [123I] β-CIT uptake also improved with increasing serum urate concentrations (overall P for trend=.002; men, P=.001; women, P=.43). Conclusions: These findings identify serum urate as the first molecular factor directly linked to the progression of typical PD and suggest that targeting urate or its determinants could be an effective disease-modifying therapy in PD.
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Schwarzschild</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital</s1><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Schwid, Steven R" sort="Schwid, Steven R" uniqKey="Schwid S" first="Steven R." last="Schwid">Steven R. 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Commentary</title><author><name sortKey="Schiess, Mya" sort="Schiess, Mya" uniqKey="Schiess M" first="Mya" last="Schiess">Mya Schiess</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Neurology, MSB 7.044, University of Texas Houston Medical Center, 6431 Fannnin St</s1><s2>Houston, TX 77030-1501</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>Houston, TX 77030-1501</wicri:noRegion></affiliation></author><author><name sortKey="Oh, Irene" sort="Oh, Irene" uniqKey="Oh I" first="Irene" last="Oh">Irene Oh</name></author><author><name sortKey="Schwarzschild, Michael A" sort="Schwarzschild, Michael A" uniqKey="Schwarzschild M" first="Michael A." last="Schwarzschild">Michael A. Schwarzschild</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital</s1><s3>USA</s3><sZ>3 aut.</sZ></inist:fA14><country>États-Unis</country><wicri:noRegion>MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Schwid, Steven R" sort="Schwid, Steven R" uniqKey="Schwid S" first="Steven R." last="Schwid">Steven R. Schwid</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Departments of Neurology and Biostatistics, University of Rochester</s1><s2>Rochester, New York</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Marek, Kenneth" sort="Marek, Kenneth" uniqKey="Marek K" first="Kenneth" last="Marek">Kenneth Marek</name><affiliation wicri:level="2"><inist:fA14 i1="04"><s1>Institute for Neurodegenerative Disorders</s1><s2>New Haven, Connecticut</s2><s3>USA</s3><sZ>5 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Connecticut</region></placeName></affiliation></author><author><name sortKey="Watts, Arthur" sort="Watts, Arthur" uniqKey="Watts A" first="Arthur" last="Watts">Arthur Watts</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Departments of Neurology and Biostatistics, University of Rochester</s1><s2>Rochester, New York</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E." last="Lang">Anthony E. Lang</name><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Toronto Western Hospital</s1><s2>Toronto, Ontario</s2><s3>CAN</s3><sZ>7 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Toronto Western Hospital</wicri:noRegion></affiliation></author><author><name sortKey="Oakes, David" sort="Oakes, David" uniqKey="Oakes D" first="David" last="Oakes">David Oakes</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Departments of Neurology and Biostatistics, University of Rochester</s1><s2>Rochester, New York</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Shoulson, Ira" sort="Shoulson, Ira" uniqKey="Shoulson I" first="Ira" last="Shoulson">Ira Shoulson</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Departments of Neurology and Biostatistics, University of Rochester</s1><s2>Rochester, New York</s2><s3>USA</s3><sZ>4 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Ascherio, Alberto" sort="Ascherio, Alberto" uniqKey="Ascherio A" first="Alberto" last="Ascherio">Alberto Ascherio</name><affiliation wicri:level="3"><inist:fA14 i1="06"><s1>Departments of Nutrition and Epidemiology, Harvard School of Public Health, and Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School</s1><s2>Boston</s2><s3>USA</s3><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><settlement type="city">Boston</settlement><region type="state">Massachusetts</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Archives of neurology : (Chicago)</title><title level="j" type="abbreviated">Arch. neurol. : (Chic.)</title><idno type="ISSN">0003-9942</idno><imprint><date when="2008">2008</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Archives of neurology : (Chicago)</title><title level="j" type="abbreviated">Arch. neurol. : (Chic.)</title><idno type="ISSN">0003-9942</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Nervous system diseases</term><term>Parkinson disease</term><term>Radiography</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Radiographie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Objective: To determine whether concentration of serum urate, a purine metabolite and potent antioxidant that has been linked to a reduced risk of Parkinson disease (PD), predicts prognosis in PD. Design: Prospective study. Setting: The Parkinson Research Examination of CEP-1347 Trial (PRECEPT) study, which investigated the effects of a potential neuroprotectant on rates of PD progression, was conducted between April 2002 and August 2005 (average follow-up time 21.4 months). Participants: Eight hundred four subjects with early PD enrolled in the PRECEPT study. Main Outcome Measures: The primary study end point was progression to clinical disability sufficient to warrant dopaminergic therapy. Cox proportional hazards models were used to estimate the hazard ratio (HR) of reaching end point according to quintiles of baseline serum urate concentration, adjusting for sex, age, and other potential covariates. Change in striatal uptake of iodine I 123-labeled 2-beta-carbomethoxy-3-beta-(4-iodophenyl) tropane ([<sup>123</sup>I] β-CIT), a marker for the presynaptic dopamine transporter, was assessed with linear regression for a subset of 399 subjects. Results: The adjusted HR of reaching end point declined with increasing baseline concentrations of urate; subjects in the top quintile reached the end point at only half the rate of subjects in the bottom quintile (HR, 0.51; 95% confidence interval [CI], 0.37-0.72; P for trend<.001). This association was markedly stronger in men (HR, 0.39; 95% CI, 0.26-0.60; P for trend <.001) than in women (HR, 0.77; 95% CI, 0.39-1.50; P for trend=.33). The percentage of loss in striatal [<sup>123</sup>I] β-CIT uptake also improved with increasing serum urate concentrations (overall P for trend=.002; men, P=.001; women, P=.43). Conclusions: These findings identify serum urate as the first molecular factor directly linked to the progression of typical PD and suggest that targeting urate or its determinants could be an effective disease-modifying therapy in PD.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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