Serum cholesterol levels and the risk of multiple system atrophy: A case‐control study
Identifieur interne : 001800 ( Main/Corpus ); précédent : 001799; suivant : 001801Serum cholesterol levels and the risk of multiple system atrophy: A case‐control study
Auteurs : Phil Hyu Lee ; Tae Sung Lim ; Hae-Won Shin ; Seok Woo Yong ; Hyo Suk Nam ; Young H. SohnSource :
- Movement Disorders [ 0885-3185 ] ; 2009-04-15.
English descriptors
Abstract
Cholesterol in brain membranes may modulate the conformational state and accumulation of α‐synuclein in α‐synucleinopathies.We examined the association between serum cholesterol and the risk of multiple system atrophy (MSA), one of the α‐synucleinopathies. We enrolled 142 patients with probable MSA from two tertiary referral hospitals and 155 age‐ and gender‐matched healthy people with no neurological disease. The levels of total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and high‐density lipoprotein cholesterol (HDL‐C) were significantly lower in MSA patients than in controls (total cholesterol: 172.7 vs. 196.3 mg/dL, P < 0.001; LDL‐C: 104.0 vs. 115.3 mg/dL, P = 0.001; HDL‐C: 47.3 vs. 54.2 mg/dL, P < 0.001). After adjusting for age, gender, use of cholesterol‐lowering drugs, and histories of hypertension, diabetes mellitus, and smoking, the odds ratios was 5.9 (95% CI = 2.3–11.5, P < 0.001) for MSA patients in the lowest quartile of total cholesterol and 2.6 (95% CI = 1.2–5.5, P = 0.016) for those in the lowest quartile of HDL‐C, compared with the highest quartiles. Levels of serum cholesterol did not significantly correlate with disease duration or severity. Our data suggest that lower levels of total cholesterol and HDL may be associated with an increased risk of MSA. © 2009 Movement Disorder Society
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DOI: 10.1002/mds.22459
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We enrolled 142 patients with probable MSA from two tertiary referral hospitals and 155 age‐ and gender‐matched healthy people with no neurological disease. The levels of total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and high‐density lipoprotein cholesterol (HDL‐C) were significantly lower in MSA patients than in controls (total cholesterol: 172.7 vs. 196.3 mg/dL, P < 0.001; LDL‐C: 104.0 vs. 115.3 mg/dL, P = 0.001; HDL‐C: 47.3 vs. 54.2 mg/dL, P < 0.001). After adjusting for age, gender, use of cholesterol‐lowering drugs, and histories of hypertension, diabetes mellitus, and smoking, the odds ratios was 5.9 (95% CI = 2.3–11.5, P < 0.001) for MSA patients in the lowest quartile of total cholesterol and 2.6 (95% CI = 1.2–5.5, P = 0.016) for those in the lowest quartile of HDL‐C, compared with the highest quartiles. Levels of serum cholesterol did not significantly correlate with disease duration or severity. Our data suggest that lower levels of total cholesterol and HDL may be associated with an increased risk of MSA. © 2009 Movement Disorder Society</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Phil Hyu Lee MD, PhD</name><affiliations><json:string>Department of Neurology, Yonsei University College of Medicine, Seoul, Korea</json:string></affiliations></json:item><json:item><name>Tae Sung Lim MD</name><affiliations><json:string>Department of Neurology, Ajou University School of Medicine, Suwon, Korea</json:string></affiliations></json:item><json:item><name>Hae‐Won Shin MD</name><affiliations><json:string>Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea</json:string></affiliations></json:item><json:item><name>Seok Woo Yong MD</name><affiliations><json:string>Department of Neurology, Ajou University School of Medicine, Suwon, Korea</json:string></affiliations></json:item><json:item><name>Hyo Suk Nam MD</name><affiliations><json:string>Department of Neurology, Yonsei University College of Medicine, Seoul, Korea</json:string></affiliations></json:item><json:item><name>Young H. 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We enrolled 142 patients with probable MSA from two tertiary referral hospitals and 155 age‐ and gender‐matched healthy people with no neurological disease. The levels of total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and high‐density lipoprotein cholesterol (HDL‐C) were significantly lower in MSA patients than in controls (total cholesterol: 172.7 vs. 196.3 mg/dL, P > 0.001; LDL‐C: 104.0 vs. 115.3 mg/dL, P = 0.001; HDL‐C: 47.3 vs. 54.2 mg/dL, P > 0.001). After adjusting for age, gender, use of cholesterol‐lowering drugs, and histories of hypertension, diabetes mellitus, and smoking, the odds ratios was 5.9 (95% CI = 2.3–11.5, P > 0.001) for MSA patients in the lowest quartile of total cholesterol and 2.6 (95% CI = 1.2–5.5, P = 0.016) for those in the lowest quartile of HDL‐C, compared with the highest quartiles. Levels of serum cholesterol did not significantly correlate with disease duration or severity. 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We enrolled 142 patients with probable MSA from two tertiary referral hospitals and 155 age‐ and gender‐matched healthy people with no neurological disease. The levels of total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and high‐density lipoprotein cholesterol (HDL‐C) were significantly lower in MSA patients than in controls (total cholesterol: 172.7 vs. 196.3 mg/dL, P < 0.001; LDL‐C: 104.0 vs. 115.3 mg/dL, P = 0.001; HDL‐C: 47.3 vs. 54.2 mg/dL, P < 0.001). After adjusting for age, gender, use of cholesterol‐lowering drugs, and histories of hypertension, diabetes mellitus, and smoking, the odds ratios was 5.9 (95% CI = 2.3–11.5, P < 0.001) for MSA patients in the lowest quartile of total cholesterol and 2.6 (95% CI = 1.2–5.5, P = 0.016) for those in the lowest quartile of HDL‐C, compared with the highest quartiles. Levels of serum cholesterol did not significantly correlate with disease duration or severity. Our data suggest that lower levels of total cholesterol and HDL may be associated with an increased risk of MSA. © 2009 Movement Disorder Society</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>multiple system atrophy</term></item><item><term>total cholesterol</term></item><item><term>HDL‐cholesterol</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2008-10-13">Received</change><change when="2008-12-21">Registration</change><change when="2009-04-15">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/8B4302F9CD6DEAA346E99C7B6C798A8B481EECBE/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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type="main" xml:lang="en"><title type="main">Abstract</title><p>Cholesterol in brain membranes may modulate the conformational state and accumulation of α‐synuclein in α‐synucleinopathies.We examined the association between serum cholesterol and the risk of multiple system atrophy (MSA), one of the α‐synucleinopathies. We enrolled 142 patients with probable MSA from two tertiary referral hospitals and 155 age‐ and gender‐matched healthy people with no neurological disease. The levels of total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and high‐density lipoprotein cholesterol (HDL‐C) were significantly lower in MSA patients than in controls (total cholesterol: 172.7 vs. 196.3 mg/dL, <i>P</i> < 0.001; LDL‐C: 104.0 vs. 115.3 mg/dL, <i>P</i> = 0.001; HDL‐C: 47.3 vs. 54.2 mg/dL, <i>P</i> < 0.001). After adjusting for age, gender, use of cholesterol‐lowering drugs, and histories of hypertension, diabetes mellitus, and smoking, the odds ratios was 5.9 (95% CI = 2.3–11.5, <i>P</i> < 0.001) for MSA patients in the lowest quartile of total cholesterol and 2.6 (95% CI = 1.2–5.5, <i>P</i> = 0.016) for those in the lowest quartile of HDL‐C, compared with the highest quartiles. Levels of serum cholesterol did not significantly correlate with disease duration or severity. Our data suggest that lower levels of total cholesterol and HDL may be associated with an increased risk of MSA. © 2009 Movement Disorder Society</p></abstract></abstractGroup></contentMeta><noteGroup><note xml:id="fn1"><p>Potential conflict of interest: Nothing to report.</p></note></noteGroup></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Serum cholesterol levels and the risk of multiple system atrophy: A case‐control study</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>The Risk of Multiple System Atrophy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Serum cholesterol levels and the risk of multiple system atrophy: A case‐control study</title></titleInfo><name type="personal"><namePart type="given">Phil Hyu</namePart><namePart type="family">Lee</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Yonsei University College of Medicine, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tae Sung</namePart><namePart type="family">Lim</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ajou University School of Medicine, Suwon, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hae‐Won</namePart><namePart type="family">Shin</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seok Woo</namePart><namePart type="family">Yong</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Ajou University School of Medicine, Suwon, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hyo Suk</namePart><namePart type="family">Nam</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Department of Neurology, Yonsei University College of Medicine, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Young H.</namePart><namePart type="family">Sohn</namePart><namePart type="termsOfAddress">MD, PhD</namePart><affiliation>Department of Neurology, Yonsei University College of Medicine, Seoul, Korea</affiliation><description>Correspondence: Department of Neurology, Yonsei University College of Medicine, 134 Shinchon‐dong, Seodaemun‐gu, Seoul 120‐752, South Korea</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">2009-04-15</dateIssued><dateCaptured encoding="w3cdtf">2008-10-13</dateCaptured><dateValid encoding="w3cdtf">2008-12-21</dateValid><copyrightDate encoding="w3cdtf">2009</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">2</extent><extent unit="references">37</extent><extent unit="words">5429</extent></physicalDescription><abstract lang="en">Cholesterol in brain membranes may modulate the conformational state and accumulation of α‐synuclein in α‐synucleinopathies.We examined the association between serum cholesterol and the risk of multiple system atrophy (MSA), one of the α‐synucleinopathies. We enrolled 142 patients with probable MSA from two tertiary referral hospitals and 155 age‐ and gender‐matched healthy people with no neurological disease. The levels of total cholesterol, low‐density lipoprotein cholesterol (LDL‐C), and high‐density lipoprotein cholesterol (HDL‐C) were significantly lower in MSA patients than in controls (total cholesterol: 172.7 vs. 196.3 mg/dL, P < 0.001; LDL‐C: 104.0 vs. 115.3 mg/dL, P = 0.001; HDL‐C: 47.3 vs. 54.2 mg/dL, P < 0.001). After adjusting for age, gender, use of cholesterol‐lowering drugs, and histories of hypertension, diabetes mellitus, and smoking, the odds ratios was 5.9 (95% CI = 2.3–11.5, P < 0.001) for MSA patients in the lowest quartile of total cholesterol and 2.6 (95% CI = 1.2–5.5, P = 0.016) for those in the lowest quartile of HDL‐C, compared with the highest quartiles. Levels of serum cholesterol did not significantly correlate with disease duration or severity. Our data suggest that lower levels of total cholesterol and HDL may be associated with an increased risk of MSA. © 2009 Movement Disorder Society</abstract><note type="content">*Potential conflict of interest: Nothing to report.</note><note type="funding">Stem Cell Research Center of the 21st Century Frontier Research Program - No. SC‐4111; </note><note type="funding">Ministry of Science and Technology, Republic of Korea</note><subject lang="en"><genre>Keywords</genre><topic>multiple system atrophy</topic><topic>total cholesterol</topic><topic>HDL‐cholesterol</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2009</date><detail type="volume"><caption>vol.</caption><number>24</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>752</start><end>758</end><total>7</total></extent></part></relatedItem><identifier type="istex">8B4302F9CD6DEAA346E99C7B6C798A8B481EECBE</identifier><identifier type="DOI">10.1002/mds.22459</identifier><identifier type="ArticleID">MDS22459</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2009 Movement Disorder Society</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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