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Publication Detail
Anti-β2-glycoprotein I, anti-prothrombin and anticardiolipin antibodies in a longitudinal study of patients with systemic lupus erythematosus and the antiphospholipid syndrome
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Journal Article
  • Authors:
    Inanç M, Donohoe S, Ravirajan CT, Radway-Bright EL, Mackie I, Machin S, Isenberg DA
  • Publication date:
    01/10/1998
  • Pagination:
    1089, 1094
  • Journal:
    British Journal of Rheumatology
  • Volume:
    37
  • Issue:
    10
  • Status:
    Published
  • Print ISSN:
    0263-7103
Abstract
Objective. To determine anti-β2 glycoprotein-I (anti-β2GPI) and anti-prothrombin (anti-ProT) antibody levels, and the IgG subclass distribution of anti-β2GPI antibodies, in serial samples from patients with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS) having initial or recurrent thrombotic/neurological (T/N) events during the study period. To investigate the correlations between these antibodies and β2GPI antigen, anticardiolipin antibody (aCL), anti-double-stranded (ds) DNA, C3 levels and disease activity. Methods. Fifty serum samples were identified from seven patients with SLE who had had T/N events during the follow-up from a cohort under long-term follow-up. IgG anti-β2GPI, anti-ProT, aCL, IgG subclasses of anti-β2GPI and β2GPI antigen levels were determined by ELISA. Corresponding disease activity [British Isles Lupus Assessment Group (BILAG)], anti-dsDNA and C3 levels were compared. Results. IgG anti-β2GPI antibody levels were elevated in six of the patients before and after the T/N events with less marked fluctuations than aCL antibody levels. The predominant subclass of anti-β2GPI antibodies was IgG2 before and after the T/N events. IgG anti-ProT antibodies were negative in all cases. There was a significant but weak correlation between anti-β2GPI and aCL antibodies. No correlation was found between disease activity and IgG anti-β2GPI antibody and β2GPI antigen levels. There were fluctuations in β2GPI antigen levels and a trend to increase after T/N events was observed in some patients. Conclusion. Most of the patients with a T/N event during the study period had IgG anti-β2GPI, but not IgG anti-ProT antibodies. Many IgG aCL-negative samples were found to have IgG anti-β2GPI activity during the follow-up period. The predominant subclass of IgG anti-β2GPI was IgG2, which may have importance in the pathogenesis of APS. β2GPI antigen levels were found to be increased in some patients with SLE after T/N events. IgG anti-β2GPI antibodies may be used as an adjunctive marker of future T/N events in patients with SLE and APS with aCL antibodies and lupus anticoagulant.
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