Nonsteroidal anti-inflammatory drugs and risk of Parkinson's disease
Identifieur interne : 001997 ( PascalFrancis/Checkpoint ); précédent : 001996; suivant : 001998Nonsteroidal anti-inflammatory drugs and risk of Parkinson's disease
Auteurs : Thanh G. Ton [États-Unis] ; Susan R. Heckbert [États-Unis] ; W. T. Jr Longstreth [États-Unis] ; Mary Anne Rossing [États-Unis] ; Walter A. Kukull [États-Unis] ; Gary M. Franklin [États-Unis] ; Phillip D. Swanson [États-Unis] ; Terri Smith-Weller [États-Unis] ; Harvey Checkoway [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2006.
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Abstract
Inflammation and oxidative stress have been implicated as pathogenic mechanisms in Parkinson's disease (PD). Evidence from in vitro and animal studies suggests a possible protective role of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. We investigated the risk of PD associated with use of aspirin and nonaspirin NSAIDs in a population-based case-control study among enrollees of Group Health Cooperative, a health maintenance organization in the Seattle area. Subjects included 206 cases between ages 35 and 89 with a new diagnosis of idiopathic PD between 1992 and 2002, and 383 randomly selected controls frequency-matched by age, sex, duration of enrollment, and clinic. We obtained information on participants' age, smoking, and medical history from interview. Exposure to NSAIDs was ascertained from an automated pharmacy database. Medications filled within 5 years of the interview were excluded. After adjusting for age, sex, smoking, duration of enrollment, and clinic, the risk of PD among individuals who received nonaspirin NSAIDs between 1977 and 1992 was 0.90 (95% CI: 0.59-1.35) and 1.67 (95% CI: 0.60-4.60) between 1993 and 2002. Use of ibuprofen was not associated with PD (OR: 0.89; 95% CI: 0.60-1.32). The risk of PD associated with aspirin or aspirin-containing medications was 0.74 (95% CI: 0.49-1.12). We observed no trend in risk according to number of fills for these drugs. Our results provide only limited support for the hypothesis that use of aspirin may reduce the risk of this disease, and no indication of protection from other NSAIDs.
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<series><title level="j" type="main">Movement disorders</title>
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<keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term>
<term>Parkinson maladie</term>
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<front><div type="abstract" xml:lang="en">Inflammation and oxidative stress have been implicated as pathogenic mechanisms in Parkinson's disease (PD). Evidence from in vitro and animal studies suggests a possible protective role of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. We investigated the risk of PD associated with use of aspirin and nonaspirin NSAIDs in a population-based case-control study among enrollees of Group Health Cooperative, a health maintenance organization in the Seattle area. Subjects included 206 cases between ages 35 and 89 with a new diagnosis of idiopathic PD between 1992 and 2002, and 383 randomly selected controls frequency-matched by age, sex, duration of enrollment, and clinic. We obtained information on participants' age, smoking, and medical history from interview. Exposure to NSAIDs was ascertained from an automated pharmacy database. Medications filled within 5 years of the interview were excluded. After adjusting for age, sex, smoking, duration of enrollment, and clinic, the risk of PD among individuals who received nonaspirin NSAIDs between 1977 and 1992 was 0.90 (95% CI: 0.59-1.35) and 1.67 (95% CI: 0.60-4.60) between 1993 and 2002. Use of ibuprofen was not associated with PD (OR: 0.89; 95% CI: 0.60-1.32). The risk of PD associated with aspirin or aspirin-containing medications was 0.74 (95% CI: 0.49-1.12). We observed no trend in risk according to number of fills for these drugs. Our results provide only limited support for the hypothesis that use of aspirin may reduce the risk of this disease, and no indication of protection from other NSAIDs.</div>
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<fA11 i1="02" i2="1"><s1>HECKBERT (Susan R.)</s1>
</fA11>
<fA11 i1="03" i2="1"><s1>LONGSTRETH (W. T. JR)</s1>
</fA11>
<fA11 i1="04" i2="1"><s1>ROSSING (Mary Anne)</s1>
</fA11>
<fA11 i1="05" i2="1"><s1>KUKULL (Walter A.)</s1>
</fA11>
<fA11 i1="06" i2="1"><s1>FRANKLIN (Gary M.)</s1>
</fA11>
<fA11 i1="07" i2="1"><s1>SWANSON (Phillip D.)</s1>
</fA11>
<fA11 i1="08" i2="1"><s1>SMITH-WELLER (Terri)</s1>
</fA11>
<fA11 i1="09" i2="1"><s1>CHECKOWAY (Harvey)</s1>
</fA11>
<fA14 i1="01"><s1>Department of Epidemiology, University of Washington</s1>
<s2>Seattle, Washington</s2>
<s3>USA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="02"><s1>Department of Neurology, University of Washington</s1>
<s2>Seattle, Washington</s2>
<s3>USA</s3>
<sZ>3 aut.</sZ>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="03"><s1>Division of Public Health Sciences, Fred Hutchinson Cancer Research Center</s1>
<s2>Seattle, Washington</s2>
<s3>USA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>Department of Environmental and Occupational Health Sciences, Seattle, University of Washington</s1>
<s2>Washington</s2>
<s3>USA</s3>
<sZ>6 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA20><s1>964-969</s1>
</fA20>
<fA21><s1>2006</s1>
</fA21>
<fA23 i1="01"><s0>ENG</s0>
</fA23>
<fA43 i1="01"><s1>INIST</s1>
<s2>20953</s2>
<s5>354000133412770130</s5>
</fA43>
<fA44><s0>0000</s0>
<s1>© 2006 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45><s0>19 ref.</s0>
</fA45>
<fA47 i1="01" i2="1"><s0>06-0393858</s0>
</fA47>
<fA60><s1>P</s1>
</fA60>
<fA61><s0>A</s0>
</fA61>
<fA64 i1="01" i2="1"><s0>Movement disorders</s0>
</fA64>
<fA66 i1="01"><s0>USA</s0>
</fA66>
<fC01 i1="01" l="ENG"><s0>Inflammation and oxidative stress have been implicated as pathogenic mechanisms in Parkinson's disease (PD). Evidence from in vitro and animal studies suggests a possible protective role of nonsteroidal anti-inflammatory drugs (NSAIDs), including aspirin. We investigated the risk of PD associated with use of aspirin and nonaspirin NSAIDs in a population-based case-control study among enrollees of Group Health Cooperative, a health maintenance organization in the Seattle area. Subjects included 206 cases between ages 35 and 89 with a new diagnosis of idiopathic PD between 1992 and 2002, and 383 randomly selected controls frequency-matched by age, sex, duration of enrollment, and clinic. We obtained information on participants' age, smoking, and medical history from interview. Exposure to NSAIDs was ascertained from an automated pharmacy database. Medications filled within 5 years of the interview were excluded. After adjusting for age, sex, smoking, duration of enrollment, and clinic, the risk of PD among individuals who received nonaspirin NSAIDs between 1977 and 1992 was 0.90 (95% CI: 0.59-1.35) and 1.67 (95% CI: 0.60-4.60) between 1993 and 2002. Use of ibuprofen was not associated with PD (OR: 0.89; 95% CI: 0.60-1.32). The risk of PD associated with aspirin or aspirin-containing medications was 0.74 (95% CI: 0.49-1.12). We observed no trend in risk according to number of fills for these drugs. Our results provide only limited support for the hypothesis that use of aspirin may reduce the risk of this disease, and no indication of protection from other NSAIDs.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002B17</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B17G</s0>
</fC02>
<fC02 i1="03" i2="X"><s0>002B02B06</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Système nerveux pathologie</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Nervous system diseases</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Sistema nervioso patología</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Parkinson maladie</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Parkinson disease</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Parkinson enfermedad</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Facteur risque</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Risk factor</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Factor riesgo</s0>
<s5>09</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Antiinflammatoire non stéroïde</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Non steroidal antiinflammatory agent</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Antiinflamatorio no esteroide</s0>
<s5>10</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Acétylsalicylique acide</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Acetylsalicylic acid</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Acetilsalicilico ácido</s0>
<s2>NK</s2>
<s2>FR</s2>
<s5>11</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Inflammation</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Inflammation</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Inflamación</s0>
<s5>12</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Encéphale pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Cerebral disorder</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Encéfalo patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Extrapyramidal syndrome</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>
<fC07 i1="03" i2="X" l="ENG"><s0>Degenerative disease</s0>
<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>Système nerveux central pathologie</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>
</fC07>
<fN21><s1>261</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations><list><country><li>États-Unis</li>
</country>
<region><li>Washington (État)</li>
</region>
<settlement><li>Seattle</li>
</settlement>
<orgName><li>Université de Washington</li>
</orgName>
</list>
<tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Ton, Thanh G" sort="Ton, Thanh G" uniqKey="Ton T" first="Thanh G." last="Ton">Thanh G. Ton</name>
</region>
<name sortKey="Checkoway, Harvey" sort="Checkoway, Harvey" uniqKey="Checkoway H" first="Harvey" last="Checkoway">Harvey Checkoway</name>
<name sortKey="Checkoway, Harvey" sort="Checkoway, Harvey" uniqKey="Checkoway H" first="Harvey" last="Checkoway">Harvey Checkoway</name>
<name sortKey="Franklin, Gary M" sort="Franklin, Gary M" uniqKey="Franklin G" first="Gary M." last="Franklin">Gary M. Franklin</name>
<name sortKey="Franklin, Gary M" sort="Franklin, Gary M" uniqKey="Franklin G" first="Gary M." last="Franklin">Gary M. Franklin</name>
<name sortKey="Heckbert, Susan R" sort="Heckbert, Susan R" uniqKey="Heckbert S" first="Susan R." last="Heckbert">Susan R. Heckbert</name>
<name sortKey="Kukull, Walter A" sort="Kukull, Walter A" uniqKey="Kukull W" first="Walter A." last="Kukull">Walter A. Kukull</name>
<name sortKey="Longstreth, W T Jr" sort="Longstreth, W T Jr" uniqKey="Longstreth W" first="W. T. Jr" last="Longstreth">W. T. Jr Longstreth</name>
<name sortKey="Longstreth, W T Jr" sort="Longstreth, W T Jr" uniqKey="Longstreth W" first="W. T. Jr" last="Longstreth">W. T. Jr Longstreth</name>
<name sortKey="Rossing, Mary Anne" sort="Rossing, Mary Anne" uniqKey="Rossing M" first="Mary Anne" last="Rossing">Mary Anne Rossing</name>
<name sortKey="Rossing, Mary Anne" sort="Rossing, Mary Anne" uniqKey="Rossing M" first="Mary Anne" last="Rossing">Mary Anne Rossing</name>
<name sortKey="Smith Weller, Terri" sort="Smith Weller, Terri" uniqKey="Smith Weller T" first="Terri" last="Smith-Weller">Terri Smith-Weller</name>
<name sortKey="Swanson, Phillip D" sort="Swanson, Phillip D" uniqKey="Swanson P" first="Phillip D." last="Swanson">Phillip D. Swanson</name>
</country>
</tree>
</affiliations>
</record>
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