Volume 98, Issue 2 pp. 336-341
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Anti-platelet antibodies in patients with systemic lupus erythematosus and the primary antiphospholipid antibody syndrome: their relationship with the observed thrombocytopenia

Laurent Macchi

Laurent Macchi

UMR 5533 CNRS, Hôpital Cardiologique,

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Patrick Rispal

Patrick Rispal

Service de Médecine Interne et Maladies Infectieuses, Centre François Magendie, Hôpital du Haut-Lévèque, Pessac, France

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Gisèle Clofent-Sanchez

Gisèle Clofent-Sanchez

UMR 5533 CNRS, Hôpital Cardiologique,

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Jean-Luc Pellegrin

Jean-Luc Pellegrin

Service de Médecine Interne et Maladies Infectieuses, Centre François Magendie, Hôpital du Haut-Lévèque, Pessac, France

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Paquita Nurden

Paquita Nurden

UMR 5533 CNRS, Hôpital Cardiologique,

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Bernard Leng

Bernard Leng

Service de Médecine Interne et Maladies Infectieuses, Centre François Magendie, Hôpital du Haut-Lévèque, Pessac, France

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Alan T. Nurden

Alan T. Nurden

UMR 5533 CNRS, Hôpital Cardiologique,

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First published: 29 October 2003
Citations: 88
Dr Alan T. Nurden UMR 5533 CNRS, Hôpital Cardiologique, 33604 Pessac, France.

Abstract

The role of antiphospholipid antibodies in the pathogenesis of the thrombocytopenia observed during primary antiphospholipid antibody syndrome (APAS) and systemic lupus erythematosus (SLE) remains controversial. We have used the MAIPA test to examine the frequency and specificity of anti-platelet antibodies directed against the major platelet membrane glycoproteins (GP IIb–IIIa, GP Ib–IX, GP Ia–IIa and GP IV) in patients where SLE and APAS were associated or not with thrombocytopenia. Results were compared with a series of 26 ITP patients, 46% of whom were shown to possess anti-platelet antibodies directed against one or more of the platelet surface glycoproteins. When APAS was associated with thrombocytopenia, 7/10 patients possessed antibodies against GP IIb–IIIa and/or GP Ib–IX. For SLE patients with thrombocytopenia, 6/10 patients were shown to have antiplatelet antibodies against GP IIb–IIIa, GP Ib–IX or GP IV. In contrast, for APAS (n=11) and SLE patients (n=11) without thrombocytopenia, only one patient had an antibody directed against GP IIb–IIIa and one patient had an antibody to GP IV. Our results suggest that antibodies directed against major platelet membrane glycoproteins may play a role in the thrombocytopenia that is seen during SLE and APAS.

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