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PS4:71 Iga anti-phospholipid antibodies in swedish cases with systemic lupus erythematosus: associations with disease phenotypes, vascular events and damage accrual
  1. M Frodlund1,
  2. A Vikerfors2,
  3. G Grosso2,
  4. T Skogh1,
  5. J Wetterö1,
  6. K Elvin3,
  7. I Gunnarsson2,
  8. A Kastbom1,
  9. Ö Dahlström4,
  10. J Rönnelid5,
  11. E Svenungsson2 and
  12. C Sjöwall1
  1. 1Divisoin of Neuro and Inflammation Sciences, Department of Clinical and Experimental Medicine, Linköping University, Linköping, Sweden
  2. 2Unit of Rheumatology, Department of Medicine Solna, Karolinska University Hospital, Stockholm, Sweden
  3. 3Unit of Clinical Immunology, Department of Clinical Immunology and Transfusion Medicine, Karolinska Institutet, Stockholm, Sweden
  4. 4Swedish Institute for Disability Research, Department of Behavioural Sciences and Learning, Linköping University, Linköping, Sweden
  5. 5Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden


Objectives IgG- and IgM-class anti-cardiolipin antibodies (aCL) and lupus anticoagulant (LA) are included in the 1997 update of the American College of Rheumatology (ACR-97) systemic lupus erythematosus (SLE) classification criteria. Despite limited evidence, IgA-aCL and IgA anti-β2-glycoprotein-I (anti-β2GPI) were included among the 2012 Systemic Lupus International Collaborating Clinics classification criteria. The present study was undertaken to evaluate IgG-/IgA-/IgM-aCL and anti-β2GPI occurrence in relation to disease phenotype, smoking habits, pharmacotherapy, APS-related events, and organ damage among Swedish SLE patients.

Methods 526 SLE patients meeting ACR-97 were included. Blood donors and patients with rheumatoid arthritis or primary Sjögren’s syndrome served as controls. Serum anti-phospholipid antibodies (aPL) were analysed by enzyme-immunoassays.

Results 76 (14%) SLE cases fulfilled the Sydney APS-criteria, and at least 1 aCL/anti-β2GPI isotype (IgG/IgA/IgM) occurred in 138 SLE patients (26%). 44 (8%) of the SLE cases had IgA-aCL, of whom 20 (4%) lacked IgG-/IgM-aCL. 74 (14%) tested positive for IgA anti-β2GPI, 34 (6%) being seronegative regarding IgG/IgM anti-β2GPI. 6 (1%) had manifestations compatible with APS and were seropositive regarding IgA-aCL and/or IgA anti-β2GPI in absence of IgG/IgM-aPL and LA. Positive LA- and IgG-aPL tests associated with most APS-related events and organ damage. Exclusive IgA anti-β2GPI occurrence associated inversely with Caucasian ethnicity and photosensitivity. Nephritis, smoking, LA-positivity and statin/corticosteroid-medication associated strongly with organ damage, whereas ongoing hydroxychloroquinemedication was protective.

Conclusions IgA-aPL is not uncommon in SLE (16%). Exclusive IgA anti-β2GPI±IgA aCL associated with non-Caucasian ethnicity. IgA-aPL analysis may be of additional value among clinically suspected APS-patients testing negative for other isotypes of aPL and LA.

Abstract PS4:71 Figure 1

A: distribution of IgA aCL and IgA anti-β2GPl positive cases in the full SLE cohort. 82 (16%) of the SLE cases had IgA positivity, 44 (8%) of aCL and 74 (14%) of anti-β2GPI type. B: Distribution of lgG/A/M isotypes of aCL in the SLE cohort. 89 (17%) SLE cases were positive for at least one aCL isotype. C: Distribution of IgG/A/M isotypes of anti-β2GPl in the SLE cohort. 121 (23%) SLE cases were positive for at least one anti-β2GPI isotype. D: Distribution of exclusiveIy lgA aCL and IgA anti-β2GPl positive cases in the SLE cohort. 20 (4%) of the SLE cases had IgA positivity, 8 (2%) of aCL and 16 (3%) of anti-β2GPl type

  • SLE
  • Antiphospholipid Antibodies
  • Immunoglobulin A

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