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Article: Associations of apolipoprotein E exon 4 and lipoprotein lipase S447X polymorphisms with acute ischemic stroke and myocardial infarction

TitleAssociations of apolipoprotein E exon 4 and lipoprotein lipase S447X polymorphisms with acute ischemic stroke and myocardial infarction
Authors
KeywordsApolipoprotein E
Ischemic
Lipoprotein lipase
Polymorphism
Smoking
Issue Date2006
PublisherWalter de Gruyter GmbH & Co KG. The Journal's web site is located at http://www.degruyter.de/journals/cclm
Citation
Clinical Chemistry And Laboratory Medicine, 2006, v. 44 n. 3, p. 274-281 How to Cite?
AbstractBackground: Because apolipoprotein E (apoE) and lipopoprotein lipase (LPL) polymorphisms interact with each other and with other factors to affect lipid metabolism, we sought to determine their separate and combined effects in association with ischemic vascular disease. Methods: We performed a case-control study of 816 subjects: 246 acute ischemic stroke patients, 234 acute myocardial infarction patients, and 336 controls. APOE exon 4 and LPL S447X genotypes were determined. Results: APOE ε2 and ε4 homozygotes were increased in stroke (4.5% vs. 1.0%, p = 0.008), while in myocardial infarction the ε4 allele was increased (12.6% vs. 9.5%, p = 0.006) but ε2 was decreased (3.7% vs. 12.1%, p = 0.000006). For subjects with either APOE ε2 or ε4 alleles, LPL X alleles were increased in vascular disease (OR = 2.2, p = 0.01). LPL X alleles displayed opposite tendencies toward association with disease when subjects were divided by sex, smoking, or APOE genotype. Meta-analysis and regression analysis of previous studies supported the sex and smoking dichotomies. Conclusion: This is the first report of an association of vascular disease with an interaction of APOE exon 4 and LPL S447X genotypes. Therefore, APOE genotypes and LPL S447X interactions with apoE, sex, and smoking may affect the risk of myocardial infarction and ischemic stroke. © 2006 by Walter de Gruyter.
Persistent Identifierhttp://hdl.handle.net/10722/92593
ISSN
2015 Impact Factor: 3.017
2015 SCImago Journal Rankings: 0.873
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBaum, Len_HK
dc.contributor.authorHo, KNen_HK
dc.contributor.authorKa, SWen_HK
dc.contributor.authorTomlinson, Ben_HK
dc.contributor.authorRainer, THen_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorWing, SCen_HK
dc.contributor.authorTang, Jen_HK
dc.contributor.authorTam, WWSen_HK
dc.contributor.authorGoggins, Wen_HK
dc.contributor.authorTong, CSWen_HK
dc.contributor.authorChan, DKYen_HK
dc.contributor.authorThomas, GNen_HK
dc.contributor.authorChook, Pen_HK
dc.contributor.authorKam, SWen_HK
dc.date.accessioned2010-09-17T10:51:06Z-
dc.date.available2010-09-17T10:51:06Z-
dc.date.issued2006en_HK
dc.identifier.citationClinical Chemistry And Laboratory Medicine, 2006, v. 44 n. 3, p. 274-281en_HK
dc.identifier.issn1434-6621en_HK
dc.identifier.urihttp://hdl.handle.net/10722/92593-
dc.description.abstractBackground: Because apolipoprotein E (apoE) and lipopoprotein lipase (LPL) polymorphisms interact with each other and with other factors to affect lipid metabolism, we sought to determine their separate and combined effects in association with ischemic vascular disease. Methods: We performed a case-control study of 816 subjects: 246 acute ischemic stroke patients, 234 acute myocardial infarction patients, and 336 controls. APOE exon 4 and LPL S447X genotypes were determined. Results: APOE ε2 and ε4 homozygotes were increased in stroke (4.5% vs. 1.0%, p = 0.008), while in myocardial infarction the ε4 allele was increased (12.6% vs. 9.5%, p = 0.006) but ε2 was decreased (3.7% vs. 12.1%, p = 0.000006). For subjects with either APOE ε2 or ε4 alleles, LPL X alleles were increased in vascular disease (OR = 2.2, p = 0.01). LPL X alleles displayed opposite tendencies toward association with disease when subjects were divided by sex, smoking, or APOE genotype. Meta-analysis and regression analysis of previous studies supported the sex and smoking dichotomies. Conclusion: This is the first report of an association of vascular disease with an interaction of APOE exon 4 and LPL S447X genotypes. Therefore, APOE genotypes and LPL S447X interactions with apoE, sex, and smoking may affect the risk of myocardial infarction and ischemic stroke. © 2006 by Walter de Gruyter.en_HK
dc.languageengen_HK
dc.publisherWalter de Gruyter GmbH & Co KG. The Journal's web site is located at http://www.degruyter.de/journals/cclmen_HK
dc.relation.ispartofClinical Chemistry and Laboratory Medicineen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectApolipoprotein Een_HK
dc.subjectIschemicen_HK
dc.subjectLipoprotein lipaseen_HK
dc.subjectPolymorphismen_HK
dc.subjectSmokingen_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAllelesen_HK
dc.subject.meshApolipoprotein E4en_HK
dc.subject.meshApolipoproteins E - geneticsen_HK
dc.subject.meshExons - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHong Kongen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLipoprotein Lipase - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshMyocardial Infarction - epidemiology - geneticsen_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.subject.meshRegression Analysisen_HK
dc.subject.meshRisk Assessmenten_HK
dc.subject.meshRisk Factorsen_HK
dc.subject.meshSmokingen_HK
dc.subject.meshStroke - epidemiology - geneticsen_HK
dc.titleAssociations of apolipoprotein E exon 4 and lipoprotein lipase S447X polymorphisms with acute ischemic stroke and myocardial infarctionen_HK
dc.typeArticleen_HK
dc.identifier.emailTam, WWS: wwstam@hkucc.hku.hken_HK
dc.identifier.authorityTam, WWS=rp01378en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1515/CCLM.2006.047en_HK
dc.identifier.pmid16519597-
dc.identifier.scopuseid_2-s2.0-33644831718en_HK
dc.identifier.hkuros115675-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644831718&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume44en_HK
dc.identifier.issue3en_HK
dc.identifier.spage274en_HK
dc.identifier.epage281en_HK
dc.identifier.isiWOS:000236203000002-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridBaum, L=7103310839en_HK
dc.identifier.scopusauthoridHo, KN=11640998200en_HK
dc.identifier.scopusauthoridKa, SW=6604061643en_HK
dc.identifier.scopusauthoridTomlinson, B=16423466900en_HK
dc.identifier.scopusauthoridRainer, TH=7004489495en_HK
dc.identifier.scopusauthoridChen, X=13309974700en_HK
dc.identifier.scopusauthoridWing, SC=12771769600en_HK
dc.identifier.scopusauthoridTang, J=12771935200en_HK
dc.identifier.scopusauthoridTam, WWS=9740867000en_HK
dc.identifier.scopusauthoridGoggins, W=6701315434en_HK
dc.identifier.scopusauthoridTong, CSW=36851992000en_HK
dc.identifier.scopusauthoridChan, DKY=52463410000en_HK
dc.identifier.scopusauthoridThomas, GN=55232963400en_HK
dc.identifier.scopusauthoridChook, P=6603266983en_HK
dc.identifier.scopusauthoridKam, SW=12771185700en_HK

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