Extended Antiphospholipid Antibodies Screening in Systemic Lupus Erythematosus Patients

Author:

Dima Alina12,Caraiola Simona12,Jurcut C.3,Balanescu Eugenia2,Balanescu P.12,Ramba Doina12,Badea Camelia12,Pompilian V.12,Ionescu R.12,Baicus Anda14,Baicus C.12,Dan G. A.12

Affiliation:

1. “Carol Davila” University of Medicine and Pharmacy, Bucharest

2. “Colentina” Research Center, Colentina Clinical Hospital, Bucharest

3. “Dr. Carol Davila” Central University Emergency Military Hospital, Bucharest

4. “Cantacuzino” National Institute of Research and Development in Microbiology-Immunology, Bucharest, Romania

Abstract

Abstract Background. The antiphospholipid syndrome (APS) is one of the most encountered autoimmunity in systemic lupus erythematosus (SLE) patients and pathogenesis of these two seems to be intricate. Aim. To investigate the association of antiphospholipid antibodies (APLAs) titer with the presence of secondary APS diagnosis in SLE patients. Methods. 65 patients fulfilling the 2012 Systemic Lupus Collaborating International Clinics (SLICC) SLE’s criteria were included. The APS diagnosis was sustained according to the 2006 Sydney APS’s criteria. Three groups of patients were defined: SLE patients with secondary APS, SLE with history of positive “criteria” APLAs but without APS clinical features, respectively SLE patients without positive APLAs or clinical APS criteria. An extended APLAs panel was searched in all cases: both IgM and IgG of anticardiolipin antibodies (aCL), anti-β2 glycoprotein I antibodies (aβ2GPI), antiphosphatidylethanolamine antibodies (aPE), antiphosphatidylserine antibodies (aPS), respectively antiprothrombin antibodies (aPT). Results. Only the aβ2GPI, both IgM and IgG serotypes, had significantly higher titers in patients with SLE and secondary APS compared to no APS (with/without positive APLAs): median (min; max) 7.0 (0.0-300.0) vs. 1.0 (0.0-28.0) vs. 1.0 (0.0-12.0), respectively 3.0 (0.0-79.0) vs. 1.0 (0.0-3.0) vs. 1.0 (0.0-12.0) (p<0.001, Kruskal-Wallis test)]. Also, in regression logistic models, only the aβ2 GPI (IgG and IgM) were identified as risk factors for secondary APS diagnosis in the SLE patients: OR(95%CI) 5.9 (2.2-15.7), respectively 1.3 (1.1-1.5). In regard with the SLE markers, the IgG serotypes of the “non-criteria” APLAs analyzed (aPS, aPT, aPE) were correlated with the antiDNA titers while the IgM serotypes inversely associated with the complement C3 levels. Conclusions. IgG aβ2 GPI are accompanied by almost 6-fold increase risk of secondary APS when screening SLE patients. On the contrary, the “non-criteria” APLAs do not seem associated with the APS diagnosis in SLE patients. Some correlates of the “non-criteria” APLAs with the antiDNA and complement C3 levels were also observed.

Publisher

Walter de Gruyter GmbH

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