Abstract
PurposeAnti-phospholipid antibodies (aPL) analyzed by line immunoassay (LIA) can recognize beta2-glycoprotein I (β2GPI) domain 1 (D1) epitopes depending on β2GPI binding to distinct phospholipids. The aPL LIA was compared with consensus ELISA to investigate whether both techniques can discriminate anti-phospholipid syndrome (APS) patients from aPL-positive, systemic autoimmune rheumatic diseases (SARD) patients without clinical symptoms of APS and controls.MethodsThirty-four APS patients (14 arterial/venous thrombosis, 16 pregnancy morbidity, and 4 both), 41 patients with SARD lacking clinical APS criteria but demonstrating positivity for anti-β2GPI (aβ2GPI) IgG, and 20 healthy subjects (HS) were tested for aPL to cardiolipin (aCL), phosphatidic acid, phosphatidylcholine, phosphatidylethanolamine, phosphatidylglycerol (aPG), phosphatidylinositol, phosphatidylserine, β2GPI, prothrombin, and annexin V by LIA. Samples were also tested for aCL, aβ2GPI, aβ2GPI-domain 1 (aD1), and aβ2GPI-domains 4–5 (aD4–5) by ELISA and for lupus anti-coagulant.ResultsComparison of LIA with ELISA revealed a good agreement for the consensus criteria aPL aβ2GPI and aCL IgG (kappa = 0.69, 0.68, respectively) and a moderate agreement for IgM (kappa = 0.52, 0.49, respectively). Regarding ELISA, aD1/aD4–5 demonstrated the best performance of differentiating APS from asymptomatic SARD [area under the curve (AUC): 0.76]. aPG IgG had the best performance by LIA (AUC: 0.72) not significantly different from aD1/aD4–5. There was a good agreement for aPG IgG with aD1/aD4–5 (kappa = 0.71).ConclusionsaD1/aD4–5 (ELISA) and aPG IgG (LIA) differentiate APS from SARD patients. PG appears to interact with β2GPI of APS patients and exposes D1 thereof for disease-specific aPL binding in LIA.
Highlights
Anti-phospholipid syndrome (APS) is an autoimmune disorder, clinically characterized by arterial and/or venous thrombosis as well as pregnancy-related complications [1, 2]
Apart from one clinical criterion, the revised classification criteria require the persistent detection of anti-phospholipid antibodies such as anti-beta2 glycoprotein I, anti-cardiolipin, and/or autoantibodies interfering with coagulation [lupus anti-coagulant (LAC)] for the diagnosis of APS
To identify the aPL antibody profiles by enzyme-linked immunosorbent assay (ELISA) and line immunoassay (LIA), we tested 34 sera from patients with APS and 61 controls including 41 asymptomatic patients suffering from systemic autoimmune rheumatic diseases (SARD) and 20 healthy subjects (HS) (Table2)
Summary
Anti-phospholipid syndrome (APS) is an autoimmune disorder, clinically characterized by arterial and/or venous thrombosis as well as pregnancy-related complications [1, 2]. The APS can be primary or secondary, depending on the absence or presence of any other related systemic autoimmune. Cecilia Nalli and Valentina Somma shared first authorship. Dirk Roggenbuck and Angela Tincani shared senior authorship. The APS could be associated with a high risk of death in the rare catastrophic anti-phospholipid syndrome, a rapid and simultaneous multi-organ failure due to generalized thrombosis [3]. Apart from one clinical criterion (vascular thrombosis and/or adverse obstetric event), the revised classification criteria require the persistent detection of anti-phospholipid antibodies (aPL) such as anti-beta glycoprotein I (aβ2GPI), anti-cardiolipin (aCL), and/or autoantibodies interfering with coagulation [lupus anti-coagulant (LAC)] for the diagnosis of APS
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