title: IgA anti-beta2-glycoprotein I autoantibodies are associated with an increased risk of thromboembolic events in patients with systemic lupus erythematosus.
abstract: BACKGROUND
  The clinical utility of testing for antiphospholipid antibodies (aPL) of IgA isotype remains controversial.
  
  
  RESULTS
  To address this issue, we reasoned that if IgA aPL contribute to the clinical manifestations of the antiphospholipid syndrome, then an association with thromboembolic events should manifest in patients whose only aPL is of IgA isotype. We performed a retrospective chart review of 56 patients (31 with systemic lupus erythematosus [SLE] and 25 without SLE) whose only positive aPL was IgA anti-beta2-glycoprotein I (isolated IgA anti-beta2GPI) and compared their clinical features with 56 individually matched control patients without any aPL. Patients with isolated IgA anti-beta2GPI had a significantly increased number of thromboembolic events, as compared to controls. When patients were stratified into those with and without SLE, the association between isolated IgA anti-beta2GPI and thromboembolic events persisted for patients with SLE, but was lost for those without SLE. Titers of IgA anti-beta2GPI were significantly higher in SLE patients who suffered a thromboembolic event. Among patients with isolated IgA anti-beta2GPI, there was an increased prevalence of diseases or morbidities involving organs of mucosal immunity (i.e., gastrointestinal system, pulmonary system, and skin).
  
  
  CONCLUSIONS
  The presence of isolated IgA anti-beta2GPI is associated with an increased risk of thromboembolic events, especially among patients with SLE. IgA anti-beta2GPI is associated with an increased prevalence of morbidities involving organs of mucosal immunity.
authors.affiliation: Section of Rheumatology, Department of Medicine, University of Chicago, Chicago, Illinois, United States of America. nsweiss@medicine.bsd.uchicago.edu
authors.forename: Nadera J
authors.initials: NJ
authors.lastname: Sweiss
authors.forename: Ronghai
authors.initials: R
authors.lastname: Bo
authors.forename: Reena
authors.initials: R
authors.lastname: Kapadia
authors.forename: Deborah
authors.initials: D
authors.lastname: Manst
authors.forename: Farzan
authors.initials: F
authors.lastname: Mahmood
authors.forename: Tara
authors.initials: T
authors.lastname: Adhikari
authors.forename: Suncica
authors.initials: S
authors.lastname: Volkov
authors.forename: Maria
authors.initials: M
authors.lastname: Badaracco
authors.forename: Mary
authors.initials: M
authors.lastname: Smaron
authors.forename: Anthony
authors.initials: A
authors.lastname: Chang
authors.forename: Joseph
authors.initials: J
authors.lastname: Baron
authors.forename: Jerrold S
authors.initials: JS
authors.lastname: Levine
mesh_terms: D000328:Adult; D000368:Aged; D001323:Autoantibodies / Q000276:immunology* / Q000302:isolation & purification; D015897:Comorbidity; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D006801:Humans; D018928:Immunity, Mucosal / Q000276:immunology; D007070:Immunoglobulin A / Q000276:immunology* / Q000302:isolation & purification; D008180:Lupus Erythematosus, Systemic / Q000453:epidemiology / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D013923:Thromboembolism / Q000453:epidemiology / Q000276:immunology*; D055815:Young Adult; D053482:beta 2-Glycoprotein I / Q000276:immunology*
chemical_list: D001323:Autoantibodies; D007070:Immunoglobulin A; D053482:beta 2-Glycoprotein I
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