Thromb Haemost 1995; 73(01): 132-137
DOI: 10.1055/s-0038-1653738
Original Article
Platelets
Schattauer GmbH Stuttgart

Effect of Plasma from Patients with Primary Antiphospholipid Syndrome on Platelet Function in a Collagen Rich Perfusion System

Joan-Carles Reverter
The Servicio de Hemoterapia y Hemostasia, Hospital Clínic I Provincial, Barcelona, Spain
,
Dolors Tàssies
The Servicio de Hemoterapia y Hemostasia, Hospital Clínic I Provincial, Barcelona, Spain
,
Ginés Escolar
The Servicio de Hemoterapia y Hemostasia, Hospital Clínic I Provincial, Barcelona, Spain
,
Josep Font
1   The Unidad de Enfermedades Sistémicas del Servicio de Medicina Interna General, Hospital Clínic i Provincial, Barcelona, Spain
,
Alfonso López Soto
1   The Unidad de Enfermedades Sistémicas del Servicio de Medicina Interna General, Hospital Clínic i Provincial, Barcelona, Spain
,
Miguel Ingelmo
1   The Unidad de Enfermedades Sistémicas del Servicio de Medicina Interna General, Hospital Clínic i Provincial, Barcelona, Spain
,
Antoni Ordinas
The Servicio de Hemoterapia y Hemostasia, Hospital Clínic I Provincial, Barcelona, Spain
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Received 19. Mai 1994

Accepted after revision 14. September 1994

Publikationsdatum:
09. Juli 2018 (online)

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Summary

The effect on platelet function of plasma from 9 patients with primary antiphospholipid syndrome (PAS) with previous thrombotic episodes was investigated under flow conditions. Five asymptomatic individuals with antiphospholipid antibodies (aPL) (A-aPL) and 14 normal controls were also studied. Patients and controls plasmas were added (1:20 v/v) to anticoagulated blood and perfused through annular chambers containing collagen rich vessel segments. The interaction of platelets with vessel subendothelium was morphometrically evaluated in thin sections. An increase in both covered surface and thrombi formation was observed in perfusions in the presence of PAS-plasma (mean ± SD: 34.2% ± 9.6% and 23.2% ± 10.0% respectively) compared with control plasmas (21.4% ± 7.3% and 10.1% ± 7.7%, p<0.01). Affinity purified anticardiolipin antibodies from one PAS patient showed a similar effect when added to normal blood. In contrast, A-aPL plasma had no effect on platelet-subendothelium interaction. In parallel studies, the same plasmas were incubated with isolated normal platelets before and after activation with ADP or collagen and the binding of immunoglobulins (Ig) was determined by flow cytometry. A significantly increased binding of Ig was observed in 8 out of 9 plasmas from PAS patients when platelets had been activated with collagen but not when resting or ADP activated platelets were used. No increased Ig binding to platelets was seen using A-aPL individuals plasma. These observations might help to explain the pathophysiology of the thrombotic events occurring in patients with PAS.