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

Abstract

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°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 /im in height) covering 11.8±5.7% of the exposed SE were noted. The deposition of platelets was statistically increased (38.5 ±7.6%,

Antiphospholipid Antibodies Induce Monocyte Chemoattractant Protein-1 in Endothelial Cells

“…These clinical manifestations accompanied by the presence of aPL are recognized as the antiphospholipid syndrome (APS). Many studies were performed to determine how aPL might induce thrombus formation in vitro, and it has been suggested that inhibition of fibrinolysis (5,6) and proteins C and S (7-10), as well as activation of endothelial cells (11,12), platelets (13)(14)(15), and monocytes (14, 16 -18), may contribute to the induction process.…”

Osteonecrosis secondary to antiphospholipid syndrome: a case report, review of the literature, and treatment strategy

“…Another mechanism suggests that antiphospholipid antibodies bind to platelets and promote platelet activation [18][19][20]. Furthermore, another proposed mechanism is that antiphospholipid antibodies interact with endothelial cells and induce expression of adhesion molecules and monocyte adhesion resulting in tissue factor expression and a procoagulant state [21][22][23][24][25][26].…”

Antiphospholipid Antibodies and APS Nephropathy

“…Anti-prothrombin antibodies (aPT) have been isolated from APS patients and these antibodies, particularly aPT complexed to PS (aPT/PS), have displayed LA activity, can induce TF expression and have thrombogenic properties in vivo [31][32][33]. Several aPT also display thrombin-binding activity and in their interaction with thrombin, prevent its inactivation by antithrombin (AT), promoting thrombosis by unchecked fibrinogen and platelet activation by thrombin [34,35]. The presence of aPL with binding activity for activated factor IX (FIXa) and FXa in APS patients has also been reported, and several of these antibodies prevent the inactivation of FIXa and FXa by antithrombin [36,37].…”