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
› Author Affiliations
Further Information

Publication History

Received 19 May 1994

Accepted after revision 14 September 1994

Publication Date:
09 July 2018 (online)

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.

 
  • References

  • 1 Harris EN. Antiphospholipid antibodies. Br J Haematol 1990; 74: 1-9
  • 2 Bowie WE J, Thomson JH, Pascuzzi CA, Owen CA. Thrombosis in systemic lupus erythematosis despite circulating anticoagulants. J Clin Invest 1963; 62: 416-430
  • 3 Harris EN, Gharavi AE, Hughes GR V. Antiphospholipid antibodies. Clin Rheum Dis 1985; 11: 591-609
  • 4 Harris EN. The antiphospholipid syndrome-an introduction. In: Harris EN, Exner T, Hughes GR V, Asherson RA. (eds) Phospholipid binding antibodies. Boca Raton, Florida (USA): CRC Press: 1991: 373-386
  • 5 Triplett DA. Antiphospholipid antibodies: Proposed mechanisms of action. Am J Reprod Immunol 1992; 28: 211-215
  • 6 Carreras LO, Vermylen JG, Deman R, Spitz B, Van Asshe A. “Lupus” anticoagulant and thrombosis. Possible role of inhibition of prostacyclin formation Thromb Haemost 1982; 48: 38-40
  • 7 Branch DW, Rodgers GM. Induction of endothelial cell tissue factor activity by sera from patients with antiphospholipid syndrome: A possible mechanism of thrombosis. Am J Obst Gynecol 1993; 168: 206-210
  • 8 Keeling DM, Campbell SJ, Mackie IJ, Machin SJ, Isenberg DA. The fibrinolytic response to venous occlusion and the natural anticoagulants in patients with antiphospholipid antibodies both with and without systemic lupus erythematosus. Br J Haematol 1991; 77: 354-359
  • 9 Freyssinet JM, Cazenave JP. Lupus-like anticoagulants, modulation of the protein C pathway and thrombosis. Thromb Haemost 1987; 58: 679-681
  • 10 Schorer AE, Wickham NW, Watson KV. Lupus anticoagulant induces a selective defect in thrombin-mediated endothelial prostacyclin release and platelet aggregation. Br J Haematol 1989; 71: 399-407
  • 11 Escolar G, Font J, Reverter JC, López-Soto A, Garrido M, Cervera R, Ingelmo M, Castillo R, Ordinas A. Plasma from systemic lupus erythematosus patients with antiphospholipid antibodies promotes platelet aggregation. Studies in a perfusion system Arterioscler Thromb 1992; 12: 196-200
  • 12 Thiagarajan P, Tait JF. Collagen-induced exposure of anionic phospholipids in platelets and platelet derived microparticles. J Biol Chem 1991; 266: 24302-24307
  • 13 Mustard JF, Kinhough-Rathbone RL, Packman MA. Isolation of human platelets by centrifugation and washing. Meth Enzymol 1989; 169: 3-11
  • 14 Tan EM, Cohen AS, Fries JF, Masi AT, McShane DJ, Rothfield NE, Schaller JG, Talal N, Winchester RJ. The 1982 revised criteria for the classification of Systemic Lupus Erythematosus. Arthritis Rheum 1982; 25: 1271-1277
  • 15 Exner T, Triplett DA, Tabemer D, Machin SJ. Guidelines for testing and revised criteria for lupus anticoagulants. SSC Subcommittee for the Standardization of Lupus Anticoagulants Thromb Haemost 1991; 65: 320-322
  • 16 Loizou S, McRea JD, Rudge AC, Reynolds R, Boyle CE, Harris EN. Measurement of anti-cardiolipin antibodies by an enzyme-linked immuno-absorbent assay (ELISA): Standardization and quantification of results. Clin Exp Immunol 1985; 62: 738-745
  • 17 Cervera R, Font J, López-Soto A, Casals F, Pallarés L, Bové A, Ingelmo M, Urbano-Marquez A. Isotype distribution of anticardiolipin antibodies in systemic lupus erythematosus: Prospective analysis of a series of 100 patients. Ann Rheum Dis 1990; 49: 109-113
  • 18 Harris EN, Gharavi AE, Tincani A, Chan JK H, Englert H, Mantelli P, Allegro F, Ballestrieri G, Hughes GR V. Affinity purified anti-cardiolipin and anti-DNA antibodies. J Clin Lab Immunol 1985; 17: 155-162
  • 19 Baumgartner HR, Muggli R. Adhesion and aggregation: Morphological demonstration and quantitation “in vivo” and “in vitro”. In: Platelets in Biology and Pathology. Gordon JL. (ed) Amsterdam, The Netherlands: North-Holland Publishing Company; 1976. pp 23-60
  • 20 Baumgartner HR. Platelet interactions with collagen fibrils in flowing blood: I. Reaction of human platelets with α-chymotrypsin digested subendothelium. Thromb Haemost 1977; 37: 1-16
  • 21 Escolar G, Bastida E, Castillo R, Ordinas A. Development of a computer program to analyze the parameters of platelet-vessel wall interaction. Haemostasis 1986; 16: 8-14
  • 22 Khamashta MA, Harris EN, Gharavi AE, Derue G, Gil A, Vazquez JJ, Hughes GR V. Immune mediated mechanism for thrombosis: Antiphospholipid antibody binding to platelet membranes. Ann Rheum Dis 1988; 47: 849-854
  • 23 Arfors L, Vesterqvist O, Johnsson H, Gréen K. Increased thromboxane formation in patients with antiphospholipid syndrome. Eur J Clin Invest 1990; 20: 607-612
  • 24 Lellouche F, Martinuzzo M, Said P, Maclouf J, Carreras LO. Imbalance of thromboxane/prostacyclin biosynthesis in patients with lupus anticoagulant. Blood 1991; 78: 2894-2899
  • 25 Orlando E, Cortelazzo S, Marchetti M, Sanfratello R, Barbui T. Prolonged bleeding time in patients with lupus anticoagulant. Thromb Haemost 1992; 68: 495-499
  • 26 Ostfeld I, Dadosh-Goffer N, Borokowski S, Talmon J, Mani A, Zor U, Lahav J. Lupus anticoagulant antibodies inhibit collagen-induced adhesion and aggregation of human platelets “in vitro”. J Clin Immunol 1992; 12: 415-423
  • 27 Escolar G, Garrido M, Aznar-Salatti J, Ordinas A, Bastida E. Comparison between human umbilical artery and rabbit abdominal aorta as substrata for platelet adhesion and platelet thrombus formation under flow conditions. Blood vessels 1991; 28: 520-531
  • 28 Lin YL, Wang CT. Activation of human platelets by rabbit anticardiolipin antibodies. Blood 1992; 80: 3135-3143
  • 29 Martinuzzo ME, Maclouf J, Carreras LO, Lévy-Toledano S. Antiphospholipid antibodies enhance thrombin-induced platelet activation and thromboxane formation. Thromb Haemost 1993; 70: 667-671
  • 30 Out HJ, de Groot PG, van Vliet M, de Gast GC, Nieuwenhuis HK, Derksen RH. Antibodies to platelets in patients with anti-phospholipid antibodies. Blood 1991; 77: 2655-2659
  • 31 Biasiolo A, Pengo V. Antiphospholipid antibodies are not present in the membrane of gel-filtered platelets with IgG anticardiolipin antibodies, lupus anticoagulant and thrombosis. Blood Coagul Fibrinolysis 1993; 4: 425-428
  • 32 McNeil HP, Simpson RJ, Chesterman CN, Krilis SA. Antiphospholipid antibodies are directed against a complex antigen that includes a lipidbinding inhibitor of coagulation: (β2-Glycoprotein I (apolipoprotein H). Proc Natl Acad Sci USA 1990; 87: 4120-4124
  • 33 Pierangeli SS, Harris EN, Davis SA, DeLorenzo G. β2-Glycoprotein 1 (β2-GPl) enhances cardiolipin binding activity but is not the antigen for antiphospholipid antibodies. Br J Haematol 1992; 82: 565-570
  • 34 Arvieux J, Roussel B, Pouzol P, Colomb MG. Platelet activating properties of murine monoclonal antibodies to (β2-glycoprotein I. Thromb Haemost 1993; 70: 336-341