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Conference Paper: Is mannose binding lectin (MBL) gene polymorphism predictive of damage in systemic lupus erythematosus (SLE)?

TitleIs mannose binding lectin (MBL) gene polymorphism predictive of damage in systemic lupus erythematosus (SLE)?
Authors
Issue Date2001
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
Citation
The 65th Annual Scientific Meeting of the American College of Rhenmatology (ACR) and 36th Annual Scientific Meeting of the Association of Rheumatology Health Professionals (ARHP), San Francisco, CA, 10-15 November 2001. In Arthritis & Rheumatism, 2001, v. 44 suppl. 9, p. S246, abstract no. 1162 How to Cite?
AbstractBACKGROUND: MBL gene polymorphism leads to low serum levels of MBL. We and others have previously shown MBL insufficiency predisposes to the development of rheumatoid arthritis (RA) and SLE in different ethnic populations. In RA, MBL insufficiency is associated with severe and erosive disease. It is not known whether low MBL level causes more severe organ damage in SLE. METHODOLOGY: Patients who satisfied the ACR criteria for the classification of SLE were recruited. The clinical presentation and disease damage index as determined according to the SLICC/ACR criteria were reviewed. Serum levels of MBL were measured by ELISA. Promoter polymorphisms and codon 54 mutations of the MBL gene were determined by PCR. RESULTS: 129 SLE patients with mean6sd duration of disease of 9.266.7 (median, range57.0, 1-31 years) years were recruited. The average cumulative SLICC score was 1.261.0 (1.0, 0-8). MBL codon 54 gene mutation was detected in 40.1% (51/127) of patients and correlated with low serum MBL level (p,0.05). There were no significant differences in damage scores between patients with (group 1, n551) and without (group 2, n576) codon 54 mutation, and those with lower (,243 ng/dl) (group 3, n532) and upper (.1439 ng/dl) (group 4, n532) inter-quartile ranges of serum MBL levels. There was no correlation between MBL gene polymorphism and serum levels of MBL level and damage to specific organ system (neurological p50.5, ocular p50.34, renal p50.5). CONCLUSIONS: Although MBL gene polymorphism and MBL insufficiency predispose to the development of SLE, they are not associated with lupus disease severity.
Persistent Identifierhttp://hdl.handle.net/10722/105883
ISSN
2015 Impact Factor: 8.955
2015 SCImago Journal Rankings: 3.206

 

DC FieldValueLanguage
dc.contributor.authorMok, TMYen_HK
dc.contributor.authorIp, EWKen_HK
dc.contributor.authorLau, YLen_HK
dc.contributor.authorLo, Yen_HK
dc.contributor.authorLau, WCSen_HK
dc.date.accessioned2010-09-25T22:52:38Z-
dc.date.available2010-09-25T22:52:38Z-
dc.date.issued2001en_HK
dc.identifier.citationThe 65th Annual Scientific Meeting of the American College of Rhenmatology (ACR) and 36th Annual Scientific Meeting of the Association of Rheumatology Health Professionals (ARHP), San Francisco, CA, 10-15 November 2001. In Arthritis & Rheumatism, 2001, v. 44 suppl. 9, p. S246, abstract no. 1162en_HK
dc.identifier.issn0004-3591en_HK
dc.identifier.urihttp://hdl.handle.net/10722/105883-
dc.description.abstractBACKGROUND: MBL gene polymorphism leads to low serum levels of MBL. We and others have previously shown MBL insufficiency predisposes to the development of rheumatoid arthritis (RA) and SLE in different ethnic populations. In RA, MBL insufficiency is associated with severe and erosive disease. It is not known whether low MBL level causes more severe organ damage in SLE. METHODOLOGY: Patients who satisfied the ACR criteria for the classification of SLE were recruited. The clinical presentation and disease damage index as determined according to the SLICC/ACR criteria were reviewed. Serum levels of MBL were measured by ELISA. Promoter polymorphisms and codon 54 mutations of the MBL gene were determined by PCR. RESULTS: 129 SLE patients with mean6sd duration of disease of 9.266.7 (median, range57.0, 1-31 years) years were recruited. The average cumulative SLICC score was 1.261.0 (1.0, 0-8). MBL codon 54 gene mutation was detected in 40.1% (51/127) of patients and correlated with low serum MBL level (p,0.05). There were no significant differences in damage scores between patients with (group 1, n551) and without (group 2, n576) codon 54 mutation, and those with lower (,243 ng/dl) (group 3, n532) and upper (.1439 ng/dl) (group 4, n532) inter-quartile ranges of serum MBL levels. There was no correlation between MBL gene polymorphism and serum levels of MBL level and damage to specific organ system (neurological p50.5, ocular p50.34, renal p50.5). CONCLUSIONS: Although MBL gene polymorphism and MBL insufficiency predispose to the development of SLE, they are not associated with lupus disease severity.-
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/en_HK
dc.relation.ispartofArthritis & Rheumatismen_HK
dc.rightsArthritis & Rheumatism. Copyright © John Wiley & Sons, Inc.en_HK
dc.titleIs mannose binding lectin (MBL) gene polymorphism predictive of damage in systemic lupus erythematosus (SLE)?en_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0004-3591&volume=44&issue=9 Supple&spage=S246&epage=&date=2001&atitle=Is+mannose+binding+lectin+(MBL)+gene+polymorphism+predictive+of+damage+in+systemic+lupus+erythematosus+(SLE)?en_HK
dc.identifier.emailLau, YL: lauylung@hkucc.hku.hken_HK
dc.identifier.emailLo, Y: yloa@HKUCC.hku.hken_HK
dc.identifier.emailLau, WCS: cslau@hku.hken_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.natureLink_to_subscribed_fulltext-
dc.identifier.doi10.1002/1529-0131(200109)44:9+<::AID-ART426>3.0.CO;2-7-
dc.identifier.hkuros69765en_HK
dc.identifier.volume44en_HK
dc.identifier.issuesuppl. 9en_HK
dc.identifier.spageS246, abstract no. 1162en_HK
dc.identifier.epageS246, abstract no. 1162-

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