Thromb Haemost 1995; 73(03): 529-534
DOI: 10.1055/s-0038-1653808
Original Articles
Platelets
Schattauer GmbH Stuttgart

Comparison of the Effects of Anticardiolipin Antibodies from Patients with the Antiphospholipid Syndrome and with Syphilis on Platelet Activation and Aggregation

Andrew L Campbell
1   The Antiphospholipid Standardization Laboratory, Division of Rheumatology, KY, USA
,
Silvia S Pierangeli
1   The Antiphospholipid Standardization Laboratory, Division of Rheumatology, KY, USA
,
Samuel Wellhausen
2   James Brown Cancer Center, Department of Medicine, University of Louisville, Louisville, KY, USA
,
Nigel E Harris
1   The Antiphospholipid Standardization Laboratory, Division of Rheumatology, KY, USA
› Author Affiliations
Further Information

Publication History

Received 01 August 1994

Accepted after resubmission 28 October 1994

Publication Date:
09 July 2018 (online)

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Summary

Anticardiolipin antibodies (aCL) are induced both in the Antiphospholipid Syndrome (APS) and syphilis, but thrombosis, thrombocytopenia, and pregnancy loss occur only in the APS. Differences in specificity and function of aCL antibodies might explain clinical differences between APS and syphilis. This study compared the effects on platelet activation and aggregation of affinity purified IgG anticardiolipin antibodies from 6 patients with the APS (IgG-APS) and 5 patients with syphilis (IgG-syph). Platelet aggregation was studied by aggregometry and platelet activation by flow cytometry. In the presence of low concentrations of thrombin, ADP, or collagen, all 6 IgG-APS samples induced platelet aggregation and activation, but none of the IgG-syph samples had this effect. In the absence of platelet agonists, only 3 of 6 IgG-APS caused platelet aggregation and none caused platelet activation; IgG-syph had no effect. The IgG-APS samples but not IgG-syph bound phosphatidylserine by ELISA. We conclude that polyclonal antibodies specific for phosphatidylserine may induce platelet activation and aggregation in the presence of low concentrations of platelet agonists.