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Article: Inflammatory gene polymorphisms and susceptibility to kawasaki disease and its arterial sequelae

TitleInflammatory gene polymorphisms and susceptibility to kawasaki disease and its arterial sequelae
Authors
KeywordsArteries
Gene polymorphisms
Kawasaki disease
Issue Date2008
PublisherAmerican Academy of Pediatrics. The Journal's web site is located at http://pediatrics.aappublications.org/
Citation
Pediatrics, 2008, v. 122 n. 3, p. e608-e614 How to Cite?
AbstractOBJECTIVE. We tested the hypothesis that single-nucleotide polymorphisms of inflammatory genes C-reactive protein (CRP) and tumor necrosis factor α (TNF-α) may exert influence on susceptibility to Kawasaki disease and its arterial sequelae. METHODS. We analyzed the CRP +1444 C→T and TNF-α -308 G→A polymorphisms in 167 patients aged 8.9 ± 4.1 years with a history of Kawasaki disease (73 with and 94 without coronary aneurysms) and 124 healthy control subjects. For patients with Kawasaki disease, we further determined whether these single-nucleotide polymorphisms were associated with coronary aneurysms, carotid arterial stiffening, and intima-media thickness. RESULTS. Genotypic and allelic frequencies of CRP +1444 for T carrier and TNF-α -308 for A carrier were significantly higher in patients than in control subjects. The genotypic and allelic distributions did not differ between patients with and those without coronary aneurysms; however, patients with CRP + 1444 CT/TT genotype compared with those with a CC genotype and patients with TNF-α -308 GA/AA genotype compared with those with a GG genotype had significantly greater carotid arterial stiffness and intima-media thickness. Carriers of both CRP +1444 T allele and TNF-α -308 A allele had the highest susceptibility to Kawasaki disease and a significant trend of increased arterial stiffness and intima-media thickness compared with those who carried either 1 or none of the rare alleles. Multiple linear regression analysis identified CRP +1444 allele carrier as a significant determinant of both carotid stiffness and carotid intima-media thickness and TNF-α - 308 A allele carrier as a determinant of only intima-media thickness. CONCLUSIONS.Our findings suggest that CRP +1444 C→T and TNF-α -308 G→A polymorphisms are associated with predisposition to Kawasaki disease and, in patients with Kawasaki disease, increased carotid arterial stiffness and intima-media thickness in the long-term. Copyright © 2008 by the American Academy of Pediatrics.
Persistent Identifierhttp://hdl.handle.net/10722/59532
ISSN
2023 Impact Factor: 6.2
2023 SCImago Journal Rankings: 2.437
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, YFen_HK
dc.contributor.authorHuang, GYen_HK
dc.contributor.authorChen, SBen_HK
dc.contributor.authorLiu, XQen_HK
dc.contributor.authorXi, Len_HK
dc.contributor.authorLiang, XCen_HK
dc.contributor.authorHuang, MRen_HK
dc.contributor.authorChen, Sen_HK
dc.contributor.authorHuang, LSen_HK
dc.contributor.authorLiu, XQen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-05-31T03:52:07Z-
dc.date.available2010-05-31T03:52:07Z-
dc.date.issued2008en_HK
dc.identifier.citationPediatrics, 2008, v. 122 n. 3, p. e608-e614en_HK
dc.identifier.issn0031-4005en_HK
dc.identifier.urihttp://hdl.handle.net/10722/59532-
dc.description.abstractOBJECTIVE. We tested the hypothesis that single-nucleotide polymorphisms of inflammatory genes C-reactive protein (CRP) and tumor necrosis factor α (TNF-α) may exert influence on susceptibility to Kawasaki disease and its arterial sequelae. METHODS. We analyzed the CRP +1444 C→T and TNF-α -308 G→A polymorphisms in 167 patients aged 8.9 ± 4.1 years with a history of Kawasaki disease (73 with and 94 without coronary aneurysms) and 124 healthy control subjects. For patients with Kawasaki disease, we further determined whether these single-nucleotide polymorphisms were associated with coronary aneurysms, carotid arterial stiffening, and intima-media thickness. RESULTS. Genotypic and allelic frequencies of CRP +1444 for T carrier and TNF-α -308 for A carrier were significantly higher in patients than in control subjects. The genotypic and allelic distributions did not differ between patients with and those without coronary aneurysms; however, patients with CRP + 1444 CT/TT genotype compared with those with a CC genotype and patients with TNF-α -308 GA/AA genotype compared with those with a GG genotype had significantly greater carotid arterial stiffness and intima-media thickness. Carriers of both CRP +1444 T allele and TNF-α -308 A allele had the highest susceptibility to Kawasaki disease and a significant trend of increased arterial stiffness and intima-media thickness compared with those who carried either 1 or none of the rare alleles. Multiple linear regression analysis identified CRP +1444 allele carrier as a significant determinant of both carotid stiffness and carotid intima-media thickness and TNF-α - 308 A allele carrier as a determinant of only intima-media thickness. CONCLUSIONS.Our findings suggest that CRP +1444 C→T and TNF-α -308 G→A polymorphisms are associated with predisposition to Kawasaki disease and, in patients with Kawasaki disease, increased carotid arterial stiffness and intima-media thickness in the long-term. Copyright © 2008 by the American Academy of Pediatrics.en_HK
dc.languageengen_HK
dc.publisherAmerican Academy of Pediatrics. The Journal's web site is located at http://pediatrics.aappublications.org/en_HK
dc.relation.ispartofPediatricsen_HK
dc.subjectArteries-
dc.subjectGene polymorphisms-
dc.subjectKawasaki disease-
dc.subject.meshAllelesen_HK
dc.subject.meshC-Reactive Protein - genetics - metabolismen_HK
dc.subject.meshCarotid Artery, Common - physiopathology - ultrasonographyen_HK
dc.subject.meshChilden_HK
dc.subject.meshDNA - geneticsen_HK
dc.subject.meshElasticityen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFollow-Up Studiesen_HK
dc.subject.meshGene Frequencyen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshGenotypeen_HK
dc.subject.meshHong Kong - epidemiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIncidenceen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMucocutaneous Lymph Node Syndrome - blood - epidemiology - geneticsen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshPolymorphism, Geneticen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTumor Necrosis Factor-alpha - blood - geneticsen_HK
dc.subject.meshVascular Resistance - physiologyen_HK
dc.titleInflammatory gene polymorphisms and susceptibility to kawasaki disease and its arterial sequelaeen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1120-7507&volume=122&issue=3&spage=608&epage=614&date=2008&atitle=Inflammatory+Gene+Polymorphisms+and+Susceptibility+to+Kawasaki+Disease+and+Its+Arterial+Sequelaeen_HK
dc.identifier.emailCheung, YF:xfcheung@hku.hken_HK
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_HK
dc.identifier.authorityCheung, YF=rp00382en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1542/peds.2008-0646en_HK
dc.identifier.pmid18710885en_HK
dc.identifier.scopuseid_2-s2.0-51649085882en_HK
dc.identifier.hkuros150413en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-51649085882&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume122en_HK
dc.identifier.issue3en_HK
dc.identifier.spagee608en_HK
dc.identifier.epagee614en_HK
dc.identifier.eissn1098-4275-
dc.identifier.isiWOS:000258822600063-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, YF=7202111067en_HK
dc.identifier.scopusauthoridHuang, GY=13309093700en_HK
dc.identifier.scopusauthoridChen, SB=12779030300en_HK
dc.identifier.scopusauthoridLiu, XQ=24780811900en_HK
dc.identifier.scopusauthoridXi, L=36837231300en_HK
dc.identifier.scopusauthoridLiang, XC=12803290200en_HK
dc.identifier.scopusauthoridHuang, MR=7404261271en_HK
dc.identifier.scopusauthoridChen, S=12780323400en_HK
dc.identifier.scopusauthoridHuang, LS=37099491400en_HK
dc.identifier.scopusauthoridLiu, XQ=12545657000en_HK
dc.identifier.scopusauthoridChan, KW=8587755300en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.citeulike3154382-
dc.identifier.issnl0031-4005-

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