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AB0652 Profiling of antiphospholipid antibodies – association with clinical symptoms in follow-up samples of APS patients
  1. D. Roggenbuck1,2,
  2. K. Egerer3,
  3. T. Buettner2,
  4. B. Lehmann3,
  5. E. Feist3,
  6. G.-R. Burmester3,
  7. T. Dörner3
  1. 1Faculty of Science, University of Applied Sciences, Senftenberg
  2. 2R/D, GA Generic Assays GmbH, Berlin/Dahlewitz
  3. 3Department of Rheumatology and Clinical Immunology, Charité-Universitätsmedizin Berlin, Berlin, Germany


Background Patients with antiphospholipid syndrome (APS) may develop during the course of disease several antiphospholipid antibodies (aPL). Such aPL antibody profiles are suggested to be associated with particular clinical symptoms.

Objectives Assessment of aPL antibody profiles by line immunodot technique employing a novel hydrophobic surface was related to clinical symptoms in follow-up samples of APS patients treated at the Charité Hospital, Universitätsmedizin Berlin.

Methods Serum samples of 45 APS patients (41 females, 4 males, median age 45 years) with at least 3 follow-up samples collected over period of up to 10 years were collected. A total of 223 serum samples were tested by line immunodot assay (LIA) for aPL IgG and IgM antibodies to phosphatidylserine (PS), phosphatidylinositol (PI), cardiolipin (CL), and beta2-glycoprotein I (β2GPI) (GA Generic Assays GmbH, Germany). Of the 45 APS patients 3 (6.7%) with a total of 20 follow-up samples had pregnancy morbidity (PM), 28 patients (62.2%) with 128 samples demonstrated deep venous thrombosis (DVT), 10 patients (22.2%) with 57 samples exhibited cerebrovascular events (CE) comprising cerebral transient ischemic attack and/or ischemic stroke, and 4 patients (8.9%) with 18 samples had pulmonary embolism (PE).

Results Within these follow-up samples, anti-PI IgM (16/57), anti-PS IgM (38/57), anti-CL IgM (45/57), and anti-β2GPI IgM (35/57) were detected by the LIA and demonstrated a substantially higher prevalence in APS patients suffering from CE compared with the remaining APS patients (P <0.01; respectively). In contrast, anti-PS IgG (18/20) and anti-β2GPI IgG (19/20) showed a significant higher prevalence in APS patients with PM (P <0.001; respectively). The prevalence of IgM to PS (0/20), CL (2/18), and β2GPI (4/16) was significantly diminished in this group (P <0.02; respectively).

The detection of at least 1, 2 or 3 aPL IgG antibodies by LIA also revealed a significant higher prevalence in this APS patient cohort (18/20, 18/20, 15/20; P <0.05, respectively). The prevalence of at least 1, 2 or 3 aPL IgM antibodies was significantly reduced (4/20, 3/20, 0/20; P <0.01, respectively). In contrast, APS patients with CE demonstrated a higher prevalence of at least 1, 2, 3 or 4 aPL IgM antibodies 48/57, 40/57, 33/57, 13/57; P <0.00001, respectively). During the course of disease of up to 10 years, aPL antibody profiles may change, but disappeared in just 1 of the 45 patients (2%).

Conclusions aPL antibody profiling by LIA candidate to differentiate APS patients with CE or PM from patients venous thrombotic events. The remarkable significant higher prevalence of IgM to PI, PS, CL, and β2GPI in APS patients suffering from CE and of IgG to PI and β2GPI in APS patients with PM warrants further investigation.

Disclosure of Interest D. Roggenbuck Shareholder of: GA Generic Assays GmbH, Medipan GmbH, Employee of: GA Generic Assays GmbH, Medipan GmbH, K. Egerer: None Declared, T. Buettner: None Declared, B. Lehmann: None Declared, E. Feist: None Declared, G.-R. Burmester: None Declared, T. Dörner: None Declared

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