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Article: Modulating effects of mannose binding lectin genotype on arterial stiffness in children after Kawasaki disease

TitleModulating effects of mannose binding lectin genotype on arterial stiffness in children after Kawasaki disease
Authors
Issue Date2004
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/
Citation
Pediatric Research, 2004, v. 56 n. 4, p. 591-596 How to Cite?
AbstractSystemic arterial stiffness is increased in patients after Kawasaki disease (KD). Recently, associations between mannose-binding lectin (MBL) gene mutation and coronary complications in infants with KD and atherosclerosis in adults have been reported. We tested the hypothesis that MBL genotype modulates arterial stiffness in children after KD. Seventy-one KD patients (42 with and 29 without coronary aneurysms), aged 9.5 ± 3.7 y, and 41 age-matched controls were studied. We determined and compared their blood pressure, brachioradial arterial stiffness as determined by pulse wave velocity (PWV), fasting total cholesterol, serum MBL level, and MBL genotype. Additionally, the modulating effects of different MBL expression genotypes [high level (HL) versus intermediate or low level (IL/LL)] on arterial stiffness in different groups were assessed. The MBL genotype distributions did not differ between patients and controls (p = 0.41) or between patients with and without coronary aneurysms (p = 0.42). Patients with IL/LL expression genotypes had significantly faster PWV than those with HL expression genotypes (7.93 ± 1.38 m/s versus 6.67 ± 2.28 m/s, p = 0.027). This genotype-modulating effect is more pronounced in patients without (HL 8.86 ± 0.77 m/s versus IL/LL 6.48 ± 2.32 m/s, p = 0.02) than those with (HL 7.50 ± 1.41 m/s versus IL/LL 6.80 ± 2.28 m/s, p = 0.32) coronary aneurysms. Multiple linear regresion analysis identified age (β = 0.26, p = 0.012), being a Kawasaki patient (β = 0.22, p = 0.015), and MBL IL/LL genotype subgroup (β = 0.20, p = 0.03) as significant determinants of arterial stiffness in the entire cohort. In conclusion, MBL genotype modulates arterial stiffness, an important cardiovascular risk factor, in children after KD.
Persistent Identifierhttp://hdl.handle.net/10722/80104
ISSN
2015 Impact Factor: 2.761
2015 SCImago Journal Rankings: 1.290
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, YFen_HK
dc.contributor.authorHo, MHKen_HK
dc.contributor.authorIp, WKen_HK
dc.contributor.authorFok, SFSen_HK
dc.contributor.authorYung, TCen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-09-06T08:02:27Z-
dc.date.available2010-09-06T08:02:27Z-
dc.date.issued2004en_HK
dc.identifier.citationPediatric Research, 2004, v. 56 n. 4, p. 591-596en_HK
dc.identifier.issn0031-3998en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80104-
dc.description.abstractSystemic arterial stiffness is increased in patients after Kawasaki disease (KD). Recently, associations between mannose-binding lectin (MBL) gene mutation and coronary complications in infants with KD and atherosclerosis in adults have been reported. We tested the hypothesis that MBL genotype modulates arterial stiffness in children after KD. Seventy-one KD patients (42 with and 29 without coronary aneurysms), aged 9.5 ± 3.7 y, and 41 age-matched controls were studied. We determined and compared their blood pressure, brachioradial arterial stiffness as determined by pulse wave velocity (PWV), fasting total cholesterol, serum MBL level, and MBL genotype. Additionally, the modulating effects of different MBL expression genotypes [high level (HL) versus intermediate or low level (IL/LL)] on arterial stiffness in different groups were assessed. The MBL genotype distributions did not differ between patients and controls (p = 0.41) or between patients with and without coronary aneurysms (p = 0.42). Patients with IL/LL expression genotypes had significantly faster PWV than those with HL expression genotypes (7.93 ± 1.38 m/s versus 6.67 ± 2.28 m/s, p = 0.027). This genotype-modulating effect is more pronounced in patients without (HL 8.86 ± 0.77 m/s versus IL/LL 6.48 ± 2.32 m/s, p = 0.02) than those with (HL 7.50 ± 1.41 m/s versus IL/LL 6.80 ± 2.28 m/s, p = 0.32) coronary aneurysms. Multiple linear regresion analysis identified age (β = 0.26, p = 0.012), being a Kawasaki patient (β = 0.22, p = 0.015), and MBL IL/LL genotype subgroup (β = 0.20, p = 0.03) as significant determinants of arterial stiffness in the entire cohort. In conclusion, MBL genotype modulates arterial stiffness, an important cardiovascular risk factor, in children after KD.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/en_HK
dc.relation.ispartofPediatric Researchen_HK
dc.rightsPediatric Research. Copyright © Lippincott Williams & Wilkins.en_HK
dc.titleModulating effects of mannose binding lectin genotype on arterial stiffness in children after Kawasaki diseaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0031-3998&volume=56&issue=4&spage=591&epage=596&date=2004&atitle=Modulating+Effects+of+Mannose+Binding+Lectin+Genotype+on+Arterial+Stiffness+in+Children+After+Kawasaki+Diseaseen_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.doi10.1203/01.PDR.0000139406.22305.A4en_HK
dc.identifier.pmid15295097-
dc.identifier.scopuseid_2-s2.0-4644252219en_HK
dc.identifier.hkuros95197en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4644252219&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume56en_HK
dc.identifier.issue4en_HK
dc.identifier.spage591en_HK
dc.identifier.epage596en_HK
dc.identifier.isiWOS:000224005000012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, YF=7202111067en_HK
dc.identifier.scopusauthoridHo, MHK=8925896400en_HK
dc.identifier.scopusauthoridIp, WK=35991732900en_HK
dc.identifier.scopusauthoridFok, SFS=7005182792en_HK
dc.identifier.scopusauthoridYung, TC=9132842300en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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