Please use this identifier to cite or link to this item: https://repository.monashhealth.org/monashhealthjspui/handle/1/29484
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dc.contributor.authorYap K.S.en
dc.contributor.authorHoi, Albertaen
dc.contributor.authorMorand, Ericen
dc.date.accessioned2021-05-14T09:58:14Zen
dc.date.available2021-05-14T09:58:14Zen
dc.date.copyright2012en
dc.date.created20130226en
dc.date.issued2013-02-28en
dc.identifier.citationArthritis and Rheumatism. Conference: Annual Scientific Meeting of the American College of Rheumatology and Association of Rheumatology Health Professionals 2012. Washington, DC United States. Conference Publication: (var.pagings). 64 (SUPPL. 10) (pp S955-S956), 2012. Date of Publication: October 2012.en
dc.identifier.issn0004-3591en
dc.identifier.urihttps://repository.monashhealth.org/monashhealthjspui/handle/1/29484en
dc.description.abstractBackground/Purpose: Previous cross-sectional studies suggest that low vitamin D may be associated with higher disease activity in SLE. Vitamin D status varies with geographic location and no studies have been reported in the Southern hemisphere. The aim of this study was to determine the relationship between Vitamin D and disease activity in SLE patients in an Australian centre. Method(s): Data was collected prospectively on patients with SLE (>4 criteria) in the Monash Lupus Clinic in Melbourne Australia between January 1 2008 and January 1 2011 who had disease activity (SLEDAI-2k) and serum 25-hydroxyvitamin D concentration (VD25) measured at the same visit. Where multiple values were available, the assessment with lowest VD25 was used (n=119). Result(s): Patients with VD25 in the lowest quartile had significantly higher SLEDAI (7.7+/-1.3) compared to those in the highest quartile (3.9+/-0.8, p=0.014). Accordingly, VD25 deficiency (VD25>=40, n=28) was associated with significantly increased SLEDAI (7.7+/-1.3) compared to patients with VD25 >40 (4.8+/-0.6, P=0.02). The relative risk of high disease activity (SLEDAI>8) for patients with VD25 deficiency was 1.6 (95% CI 1.1-2.2, P=0.002). In parallel, high disease activity was associated with significantly lower VD25 compared to patients with SLEDAI<8 (P= 0.048) or patients with inactive disease (SLEDAI<4, P=0.0073). When assessing all values, a significant negative correlation between SLEDAI and VD25 was observed (Spearman r =0.2, p =0.03). There was no association of VD25 with corticosteroid use, SLICC SLE Damage Index (SDI), or ethnicity.Vitamin D supplement use (n=53) was significantly more common among patients using corticosteroids (P=0.0001) and was associated with significantly higher VD25 (P=0.009). However, there was no association between Vitamin D supplementation and SLEDAI. Conclusion(s): In a cohort of Australian patients with SLE, Vitamin D correlates negatively with disease activity. Prospective studies should examine the predictive value of Vitamin D levels and therapeutic effect of Vitamin D.en
dc.languageEnglishen
dc.languageenen
dc.publisherJohn Wiley and Sons Inc.en
dc.titleAssociation of low vitamin d with high disease activity in an australian systemic lupus erythematosus cohort.en
dc.typeConference Abstracten
dc.identifier.affiliationRheumatology-
dc.type.studyortrialObservational study (cohort, case-control, cross sectional or survey)-
dc.identifier.doihttp://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1002/art.37735en
local.date.conferencestart2012-11-09en
dc.identifier.source71000253en
dc.identifier.institution(Yap) Monash Medical Centre, Clayton, Australia (Hoi, Morand) Monash University, Melbourne, Australiaen
dc.description.addressK.S. Yap, Monash Medical Centre, Clayton, Australiaen
dc.description.publicationstatusCONFERENCE ABSTRACTen
local.date.conferenceend2012-11-14en
dc.rights.statementCopyright 2013 Elsevier B.V., All rights reserved.en
dc.identifier.affiliationext(Hoi, Morand) Monash University, Melbourne, Australia-
dc.identifier.affiliationmh(Yap) Monash Medical Centre, Clayton, Australia-
item.fulltextNo Fulltext-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.openairetypeConference Abstract-
item.cerifentitytypePublications-
item.grantfulltextnone-
crisitem.author.deptRheumatology-
crisitem.author.deptRheumatology-
crisitem.author.deptCentre for Inflammatory Diseases at Monash Health-
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