Arteriosclerosis and Thrombosis, Vol 12, 196-200, Copyright © 1992 by American Heart Association

ARTICLES

Plasma from systemic lupus erythematosus patients with antiphospholipid antibodies promotes platelet aggregation. Studies in a perfusion system

G Escolar, J Font, JC Reverter, A Lopez-Soto, M Garrido, R Cervera, M Ingelmo, R Castillo and A Ordinas
Servicio de Hemoterapia y Hemostasia, Hospital Clinic i Provincial, Barcelona, Spain.

The possible platelet-aggregating effect of plasma from systemic lupus erythematosus (SLE) patients (n = 19) was investigated under flow conditions. Aliquots of the SLE plasmas with (n = 10) or without (n = 9) anticardiolipin antibodies (ACAs) were added to anticoagulated blood (1:20, vol/vol). Plasma from normal donors was used as a control. Blood was incubated for 15 minutes at 37 degrees C and then perfused through annular chambers containing denuded arterial segments. Perfusions were performed for 10 minutes at a shear rate of 800 sec-1. The interaction of platelets with vessel subendothelium (SE) was morphometrically evaluated in thin sections. In control experiments, the percentage of the SE covered with platelets was 23.6 +/- 4.3% (mean +/- SD). Large aggregates (more than 5 microns in height) covering 11.8 +/- 5.7% of the exposed SE were noted. The deposition of platelets was statistically increased (38.5 +/- 7.6%, p less than 0.01 versus control) in the presence of SLE plasmas with demonstrated antiphospholipid antibodies (APAs). The formation of large aggregates was also augmented (30.3 +/- 5.9%, p less than 0.01 versus control). A similar response was obtained after addition of affinity-purified immunoglobulin G and immunoglobulin M fractions from two patients with ACAs. SLE plasmas with no detectable APAs did not influence the morphometric parameters studied. Results of the present study indicate that the presence of APAs in SLE plasma promotes platelet aggregation under flow conditions. These observations may help to explain the pathophysiology of the thrombotic events occurring in patients with APAs.

This article has been cited by other articles:

				P. Chen, C. Yang, K Ede, C. Wu, J. FitzGerald, and J. Grossman Some antiphospholipid antibodies bind to hemostasis and fibrinolysis proteases and promote thrombosis Lupus, October 1, 2008; 17(10): 916 - 921. [Abstract] [PDF]

				S. E. ElChoufani, P. Bolin, S. Waien, C. R. Christiano, D. Holbert, and A. P. Bode Platelet Adhesion Testing May Predict Early Hemodialysis Arteriovenous Graft and Fistula Failure in End-Stage Renal Disease Patients Clinical and Applied Thrombosis/Hemostasis, October 1, 2008; 14(4): 399 - 409. [Abstract] [PDF]

				C.-S. Cho, M.-L. Cho, P. P. Chen, S.-Y. Min, S.-Y. Hwang, K.-S. Park, W.-U. Kim, D.-J. Min, J.-K. Min, S.-H. Park, et al. Antiphospholipid Antibodies Induce Monocyte Chemoattractant Protein-1 in Endothelial Cells J. Immunol., April 15, 2002; 168(8): 4209 - 4215. [Abstract] [Full Text] [PDF]

				M. A. CASAO, R. DIAZ, A. ORDUNA, and C. GAMAZO Promotion of platelet aggregation by sera from brucellosis patients with antiphosphatidylcholine antibodies J. Med. Microbiol., November 1, 2001; 50(11): 965 - 968. [Abstract] [Full Text] [PDF]

				S. K. Srinivasan, M. R. Pittelkow, and L. T. Cooper JR Recombinant Tissue Plasminogen Activator for the Treatment of Cutaneous Infarctions in Antiphospholipid Antibody Syndrome: A Case Report Angiology, September 1, 2001; 52(9): 635 - 639. [Abstract] [PDF]

				J E Joseph, S Donohoe, P Harrison, I J Mackie, and S J Machin Platelet activation and turnover in the primary antiphospholipid syndrome Lupus, June 1, 1998; 7(5): 333 - 340. [Abstract] [PDF]

				J. Joseph, P. Harrison, I. Mackie, and S.J. Machin Review : Platelet activation markers and the primary antiphospholipid syndrome (PAPS) Lupus, January 1, 1998; 7(2_suppl): S48 - S51. [Abstract] [PDF]

				J.-C. Reverter, D. Tassies, J. Font, J. Monteagudo, G. Escolar, M. Ingelmo, and A. Ordinas Hypercoagulable State in Patients With Antiphospholipid Syndrome Is Related to High Induced Tissue Factor Expression on Monocytes and to Low Free Protein S Arterioscler Thromb Vasc Biol, November 1, 1996; 16(11): 1319 - 1326. [Abstract] [Full Text]

				L. Ziporen, I. Goldberg, M. Arad, M. Hojnik, J. Ordi-Ros, A. Afek, M. Blank, Y. Sandbank, M. Vilardell-Tarres, I. de Torres, et al. Libman-Sacks endocarditis in the antiphospholipid syndrome: immunopathologic findings in deformed heart valves Lupus, June 1, 1996; 5(3): 196 - 205. [Abstract] [PDF]