The value of IgA antiphospholipid testing for diagnosis of antiphospholipid (Hughes) syndrome in systemic lupus erythematosus

Objective. It is recognized that the presence of IgG and IgM anticardiolipi n antibodies (aCL) and lupus anticoagulant (LAC) is associated with thrombo sis in patients with anti phospholipid syndrome (APS). Some reports have sh own that testing for IgA anticardiolipin and anti-B-2-glycoprotein antibodi es (anti-beta (2)-GPI) provides extra diagnostic help in patients with APS, while other authors could not support this data. We designed this cross se ctional study to determine the prevalence of IgA aCL, anti-beta (2)-GPI, an d antiprothrombin antibodies and to study their clinical significance in a large cohort of patients with systemic lupus erythematosus (SLE). Methods. This study comprised 134 SLE patients (126 women median age 37.5 y rs, range 16-72). The median duration of the disease was 9 years, range 0.1 -38. Of these, 55 (41%) had a history of thrombotic events: 22 (40%) presen ted an arterial event, 22 (40%) a venous event, and 11 (20%) both arterial and venous events. Of 49 women who had been pregnant, 18 (37%) gave a histo ry of recurrent pregnancy loss. Thrombocytopenia was present in 14/127 pati ents (11%). Forty patients (30%) were diagnosed as APS secondary to SLE, 23 (17%) had IgG/M aCL and/or LAC without clinical features of APS, and 71 (5 3%) were SLE patients who were repeatedly negative for IgG/M aCL or LAC. Ig G, IgM, IgA aCL and anti-beta (2)-GPI were detected by ELISA. Antibodies di rected to prothrombin were detected by 2 ELISA using prothrombin coated on irradiated plates (aPT) and phosphatidylserine/prothrombin complex (aPS/PT) as antigen. Results. IgA aCL were found in 18/134 (13%) patients. Of these, 3 (17%) had IgA aCL as well as IgG/M aCL, and 2 (11%) had IgG/M aCL and anti-beta (2)- GPI. Of the 18 patients positive for IgA aCL, 8 were also positive for LAC. Of these, one (5%) patient had IgA aCL as well as other isotype of aCL, an d 7 (39%) patients had both aCL and anti-beta (2)-GPI. None of these patien ts had binding of IgA aPT or aPS/PT. Of the entire group of 18 patients, 5 (28%) had IgA aCL as the sole aPL. Four of 5 of these patients were diagnos ed as SLE but had no antiphospholipid (aPL) related clinical manifestations . We found no association between the presence of IgA aCL and clinical mani festations of APS. IgA anti-beta (2)-GPI were found in 8/134 (6%) patients. Of these, one (12.5%) had IgA anti-beta (2)-GPI as well as IgG/M anti-beta (2)-GPI and aCL. Of the 8 patients positive for IgA anti-beta (2)-GPI, 6 ( 75%) were also positive for LAC. Of these, one (12.5%) patient presented wi th IgA anti-beta (2)-GPI along with other isotypes of aCL, and 4 (50%) pati ents with aCL and other isotype of anti-beta (2)-GPI. One patient (12.5%) h ad IgA anti-beta (2)-GPI along with LAC only, and one patient (12.5%) who w as diagnosed as SLE had no aPL related clinical manifestation but had IgA a nti-beta (2)-GPI as the sole aPL. Conclusion. IgA aCL and anti-beta (2)-GPI are found in SLE, usually along w ith IgG and/or IgM isotypes. Testing for IgA aCL and anti-beta (2)-GPI is n ot a helpful screening test and does not contribute to the recognition of A PS in SLE. IgA aPT and aPS/PT are not present in patients with SLE, therefo re there is no need to test for these antibodies.