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Specificities of Platelet Autoantibodies and Platelet Activation in Lupus Anticoagulant Patients: A Relation to their History of Thromboembolic Disease

Clinic for Blood Group Serology, Medical University of Vienna, Austria, Clinic for Blood Group Serology and Transfusion Medicine, Medical University of Graz, Austria

C Rosin

Clinic for Blood Group Serology, Medical University of Vienna, Austria

R Vormittag

Department of Internal Medicine, Division of Haematology and Haemostaseology, Medical University of Vienna, Austria

M Brunner

Clinic for Blood Group Serology, Medical University of Vienna, Austria, Department for Otorhinolaryngology, Medical University of Vienna, Austria

D Dunkler

Core Unit for Medical Statistics and Informatics, Section of Clinical Biometrics, Medical University of Vienna, Austria

I Pabinger

Department of Internal Medicine, Division of Haematology and Haemostaseology, Medical University of Vienna, Austria

S Panzer

Clinic for Blood Group Serology, Medical University of Vienna, Austria, simon.panzer{at}univie.ac.at

Lupus anticoagulants (LA) prolong in vitro phospholipid-dependent coagulation tests, but are associated with thromboembolic disease (TE). However, a subgroup of individuals with LA has no TE, and it is therefore desirable to distinguish those at risk for TE from those without. Whether platelets have a primary role in the development of TE is not clear yet. We determined platelet autoantibodies to identify a specific platelet target which is associated with platelet activation in 97 patients with a long history of detectable LA, 65 patients with TE (LA/TE+), and 32 individuals without TE (LA/TE+). Thrombocytopenia was more common in the LA/TE- than in the LA/TE+ group (P < 0.05). Both groups had platelet antibodies, but the frequency of antibodies was lower in LA/TE+ than LA/TE- patients (P < 0.01), who had higher antibody titres against glycoprotein IIb/IIIa and glycoprotein Ib/IX (P < 0.05). Also, their platelets were more activated, as determined by PAC-1 binding (P < 0.01). These differences were also noted if patients with arterial thrombosis were evaluated separately. These findings in LA/TE- individuals were similar to those in patients with chronic autoimmune thrombocytopenia. However, there was no autoantibody target identifiable to distinguish between LA/TE- from LA-TE+ individuals. We therefore conclude that the presence of platelet antibodies, even if associated with platelet activation, is not sufficient to dispose LA patients to thromboembolic disease.

Key Words: lupus anticoagulant • platelet activation • platelet autoantibodies • thromboembolic disease

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