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dc.contributor.authorElkhalifa, Marwa
dc.contributor.authorOrbai, Ana-Maria
dc.contributor.authorMagder, Laurence S
dc.contributor.authorPetri, Michelle
dc.contributor.authorAlarcón, Graciela S
dc.contributor.authorGordon, Caroline
dc.contributor.authorMerrill, Joan
dc.contributor.authorFortin, Paul R
dc.contributor.authorBruce, Ian N
dc.contributor.authorIsenberg, David
dc.contributor.authorWallace, Daniel
dc.contributor.authorNived, Ola
dc.contributor.authorRamsey-Goldman, Rosalind
dc.contributor.authorBae, Sang-Cheol
dc.contributor.authorHanly, John G
dc.contributor.authorSanchez-Guerrero, Jorge
dc.contributor.authorClarke, Ann E
dc.contributor.authorAranow, Cynthia
dc.contributor.authorManzi, Susan
dc.contributor.authorUrowitz, Murray
dc.contributor.authorGladman, Dafna D
dc.contributor.authorKalunian, Ken
dc.contributor.authorWerth, Victoria P
dc.contributor.authorZoma, Asad
dc.contributor.authorBernatsky, Sasha
dc.contributor.authorKhamashta, Munther
dc.contributor.authorJacobsen, Søren
dc.contributor.authorBuyon, Jill P
dc.contributor.authorDooley, Mary Anne
dc.contributor.authorVollenhoven, Ronald van
dc.contributor.authorGinzler, Ellen
dc.contributor.authorStoll, Thomas
dc.contributor.authorPeschken, Christine
dc.contributor.authorJorizzo, Joseph L
dc.contributor.authorCallen, Jeffery P
dc.contributor.authorLim, Sam
dc.contributor.authorInanc, Murat
dc.contributor.authorKamen, Diane L
dc.contributor.authorRahman, Anisur
dc.contributor.authorSteinsson, Kristjan
dc.contributor.authorFranks, Andrew G
dc.date.accessioned2023-02-08T20:44:15Z
dc.date.available2023-02-08T20:44:15Z
dc.date.issued2021-05-06
dc.identifier.citationElkhalifa M, Orbai AM, Magder LS, Petri M, Alarcón GS, Gordon C, Merrill J, Fortin PR, Bruce IN, Isenberg D, Wallace D, Nived O, Ramsey-Goldman R, Bae SC, Hanly JG, Sanchez-Guerrero J, Clarke AE, Aranow C, Manzi S, Urowitz M, Gladman DD, Kalunian K, Werth VP, Zoma A, Bernatsky S, Khamashta M, Jacobsen S, Buyon JP, Dooley MA, Vollenhoven RV, Ginzler E, Stoll T, Peschken C, Jorizzo JL, Callen JP, Lim S, Inanc M, Kamen DL, Rahman A, Steinsson K, Franks AG Jr. Anti-beta 2 glycoprotein I IgA in the SLICC classification criteria dataset. Lupus. 2021 Jul;30(8):1283-1288. doi: 10.1177/09612033211014248. Epub 2021 May 6. PMID: 33957797.en_US
dc.identifier.eissn1477-0962
dc.identifier.doi10.1177/09612033211014248
dc.identifier.pmid33957797
dc.identifier.urihttp://hdl.handle.net/20.500.12648/8313
dc.description.abstractAnti-beta 2 glycoprotein I IgA is a common isotype of anti-beta 2 glycoprotein I in SLE. Anti-beta 2 glycoprotein I was not included in the American College of Rheumatology (ACR) SLE classification criteria, but was included in the Systemic Lupus International Collaborating Clinics (SLICC) criteria. We aimed to evaluate the prevalence of anti-beta 2-glycoprotein I IgA in SLE versus other rheumatic diseases. In addition, we examined the association between anti-beta 2 glycoprotein I IgA and disease manifestations in SLE.
dc.description.abstractThe dataset consisted of 1384 patients, 657 with a consensus physician diagnosis of SLE and 727 controls with other rheumatic diseases. Anti-beta 2 glycoprotein I isotypes were measured by ELISA. Patients with a consensus diagnosis of SLE were compared to controls with respect to presence of anti-beta 2 glycoprotein I. Among patients with SLE, we assessed the association between anti-beta 2 glycoprotein I IgA and clinical manifestations.
dc.description.abstractThe prevalence of anti-beta 2 glycoprotein I IgA was 14% in SLE patients and 7% in rheumatic disease controls (odds ratio, OR 2.3, 95% CI: 1.6, 3.3). It was more common in SLE patients who were younger patients and of African descent (p = 0.019). Eleven percent of SLE patients had anti-beta 2 glycoprotein I IgA alone (no anti-beta 2 glycoprotein I IgG or IgM). There was a significant association between anti-beta 2 glycoprotein I IgA and anti-dsDNA (p = 0.001) and the other antiphospholipid antibodies (p = 0.0004). There was no significant correlation of anti-beta 2 glycoprotein I IgA with any of the other ACR or SLICC clinical criteria for SLE. Those with anti-beta 2 glycoprotein I IgA tended to have a history of thrombosis (12% vs 6%, p = 0.071), but the difference was not statistically significant.
dc.description.abstractWe found the anti-beta 2 glycoprotein I IgA isotype to be more common in patients with SLE and in particular, with African descent. It could occur alone without other isotypes.
dc.language.isoenen_US
dc.relation.urlhttps://journals.sagepub.com/doi/10.1177/09612033211014248en_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectSystemic lupus erythematosusen_US
dc.subjectanti-beta 2 glycoprotein IgAen_US
dc.subjectantiphospholipid antibodiesen_US
dc.subjectclassification criteriaen_US
dc.titleAnti-beta 2 glycoprotein I IgA in the SLICC classification criteria dataset.en_US
dc.typeArticle/Reviewen_US
dc.source.journaltitleLupusen_US
dc.source.volume30
dc.source.issue8
dc.source.beginpage1283
dc.source.endpage1288
dc.source.countryUnited States
dc.source.countryUnited States
dc.source.countryEngland
dc.description.versionAMen_US
refterms.dateFOA2023-02-08T20:44:16Z
html.description.abstractAnti-beta 2 glycoprotein I IgA is a common isotype of anti-beta 2 glycoprotein I in SLE. Anti-beta 2 glycoprotein I was not included in the American College of Rheumatology (ACR) SLE classification criteria, but was included in the Systemic Lupus International Collaborating Clinics (SLICC) criteria. We aimed to evaluate the prevalence of anti-beta 2-glycoprotein I IgA in SLE versus other rheumatic diseases. In addition, we examined the association between anti-beta 2 glycoprotein I IgA and disease manifestations in SLE.
html.description.abstractThe dataset consisted of 1384 patients, 657 with a consensus physician diagnosis of SLE and 727 controls with other rheumatic diseases. Anti-beta 2 glycoprotein I isotypes were measured by ELISA. Patients with a consensus diagnosis of SLE were compared to controls with respect to presence of anti-beta 2 glycoprotein I. Among patients with SLE, we assessed the association between anti-beta 2 glycoprotein I IgA and clinical manifestations.
html.description.abstractThe prevalence of anti-beta 2 glycoprotein I IgA was 14% in SLE patients and 7% in rheumatic disease controls (odds ratio, OR 2.3, 95% CI: 1.6, 3.3). It was more common in SLE patients who were younger patients and of African descent (p = 0.019). Eleven percent of SLE patients had anti-beta 2 glycoprotein I IgA alone (no anti-beta 2 glycoprotein I IgG or IgM). There was a significant association between anti-beta 2 glycoprotein I IgA and anti-dsDNA (p = 0.001) and the other antiphospholipid antibodies (p = 0.0004). There was no significant correlation of anti-beta 2 glycoprotein I IgA with any of the other ACR or SLICC clinical criteria for SLE. Those with anti-beta 2 glycoprotein I IgA tended to have a history of thrombosis (12% vs 6%, p = 0.071), but the difference was not statistically significant.
html.description.abstractWe found the anti-beta 2 glycoprotein I IgA isotype to be more common in patients with SLE and in particular, with African descent. It could occur alone without other isotypes.
dc.description.institutionSUNY Downstateen_US
dc.description.departmentRheumatologyen_US
dc.description.degreelevelN/Aen_US
dc.identifier.journalLupus


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