TY - JOUR
T1 - Anti-beta 2 glycoprotein I IgA in the SLICC classification criteria dataset
AU - Elkhalifa, Marwa
AU - Orbai, Ana Maria
AU - Magder, Laurence S.
AU - Petri, Michelle
AU - Alarcón, Graciela S.
AU - Gordon, Caroline
AU - Merrill, Joan
AU - Fortin, Paul R.
AU - Bruce, Ian N.
AU - Isenberg, David
AU - Wallace, Daniel
AU - Nived, Ola
AU - Ramsey-Goldman, Rosalind
AU - Bae, Sang Cheol
AU - Hanly, John G.
AU - Sanchez-Guerrero, Jorge
AU - Clarke, Ann E.
AU - Aranow, Cynthia
AU - Manzi, Susan
AU - Urowitz, Murray
AU - Gladman, Dafna D.
AU - Kalunian, Ken
AU - Werth, Victoria P.
AU - Zoma, Asad
AU - Bernatsky, Sasha
AU - Khamashta, Munther
AU - Jacobsen, SØren
AU - Buyon, Jill P.
AU - Dooley, Mary Anne
AU - Vollenhoven, Ronald van
AU - Ginzler, Ellen
AU - Stoll, Thomas
AU - Peschken, Christine
AU - Jorizzo, Joseph L.
AU - Callen, Jeffery P.
AU - Lim, Sam
AU - Inanc, Murat
AU - Kamen, Diane L.
AU - Rahman, Anisur
AU - Steinsson, Kristjan
AU - Franks, Andrew G.
N1 - Publisher Copyright:
© The Author(s) 2021.
PY - 2021/7
Y1 - 2021/7
N2 - Objective: Anti-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. Methods: The 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. Results: The 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. Conclusion: We 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.
AB - Objective: Anti-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. Methods: The 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. Results: The 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. Conclusion: We 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.
KW - Systemic lupus erythematosus
KW - anti-beta 2 glycoprotein IgA
KW - antiphospholipid antibodies
KW - classification criteria
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U2 - 10.1177/09612033211014248
DO - 10.1177/09612033211014248
M3 - Article
C2 - 33957797
AN - SCOPUS:85105709907
SN - 0961-2033
VL - 30
SP - 1283
EP - 1288
JO - Lupus
JF - Lupus
IS - 8
ER -