Detection of anti-bovine ?2-glycoprotein I antibody in sera from patients with antiphospholipid syndrome

Abstract

We studied and characterized anti-bovine beta 2-glycoprotein I antibodies (aB beta 2-GPI) in sera from patients with antiphospholipid syndrome (APS) by ELISA. Bovine beta 2-glycoprotein I (beta 2-GPI) was purified by heparin affinity and DEAE ion-exchange chromatography, and identified on immunoblots using a monoclonal antibody against human beta 2-GPI and by amino acid sequence analysis. aB beta 2-GPI levels in the sera from 36 APS patients were measured by ELISA using purified bovine beta 2-GPI as an antigen. The mean +/- standard deviation level of aB beta 2-GPI was 17.4 +/- 22.0 units in the 58% of APS patients who were positive. There was a significant correlation (P = 0.003) between aB beta 2-GPI and anticardiolipin antibody (aCL) levels. aB beta 2-GPI from the sera of patients with APS was inhibited by bovine beta 2-GPI itself. Purified IgG from the sera of patients with APS showed that bovine beta 2-GPI was capable of acting as a cofactor for aCL. Purified bovine beta 2-GPI was useful antigen for conventional ELISA. aB beta 2-GPI may contribute to the further development of aCL analysis and to the understanding of the pathogenesis of APS.

Is the determination of anti‐beta2 glycoprotein I antibodies useful in patients with venous thromboembolism without the antiphospholipid syndrome?

“…Recently, several reports have provided evidence that anti‐beta2GPI IgG antibodies are a marker for APLS (Viard et al , 1992; Cevallos et al , 1994; El Kadi et al , 1995; Nomura et al , 1995; Pengo et al , 1996). At present, there are insufficient data in the literature analysing the relevance of elevated anti‐beta2GPI antibody levels in patients without LA or ACA.…”

Eine Patientin mit Mischkollagenose, Antiphospholipid-Syndrom und Sjögren-Syndrom

“…Trotz ab und zu neu auftretender polemischer Meinungen ª Sinn und Unsinn der DiagnosesteUung Mischkollagenose [8,10,14] Im Bereich der m6glichen Mechanismen, die Thrombosen im R.ahmen dieses Syndroms verursachen, liegen Effekte der Antiphospholipid-Antik6rper auf die Thrombozytenmembran, auf Endothelzellen, auf Gefinnungsfaktoren wie Prothrombin, Protein C und Protein S [13]. Neuerdings wird auch Antik6rpem gegen [32-Glykoprotein I eine pathogenetische R.olle zugeschrieben [20].…”