title: Increased circulating platelet-leucocyte complexes and platelet activation in patients with antiphospholipid syndrome, systemic lupus erythematosus and rheumatoid arthritis.
abstract: It is possible that platelet activation may play a pathogenic role in the increased risk of thrombosis associated with antiphospholipid antibodies (APA). In this study, levels of in vivo platelet activation were measured in 20 patients with primary antiphospholipid syndrome (PAPS) and 30 systemic lupus erythematosus (SLE) patients (14 of whom had secondary APS) using sensitive flow cytometry. Soluble P-selectin levels were also assayed. Platelet CD63 expression was significantly higher in PAPS than normal controls (P = 0.007), as well as SLE patients with and without secondary APS (P = 0.03 and P = 0.002 respectively). PAC-1 binding was significantly higher in PAPS than the control group (P = 0.007) and SLE patients without APS (P = 0.015). Platelet-leucocyte complexes were significantly higher in SLE patients than both PAPS and the control group, and platelet-monocyte complexes were significantly increased in PAPS compared with the control group. (Platelet-leucocyte complexes were also significantly higher than controls in 10 rheumatoid arthritis (RA) patients without APA). Soluble P-selectin levels were significantly higher in PAPS and SLE patients than the control group. Platelet CD62p expression, annexin V binding and platelet microparticle numbers were not increased in PAPS or SLE patients. We conclude that there is evidence of increased platelet activation in PAPS and SLE, and this is important to note as it may have potential therapeutic implications with respect to use of antiplatelet agents in these patients.
authors.affiliation: Haemostasis Research Unit, Department of Medicine, University College London, UK. j.joseph@garvan.unsw.edu.au
authors.forename: J E
authors.initials: JE
authors.lastname: Joseph
authors.forename: P
authors.initials: P
authors.lastname: Harrison
authors.forename: I J
authors.initials: IJ
authors.lastname: Mackie
authors.forename: D A
authors.initials: DA
authors.lastname: Isenberg
authors.forename: S J
authors.initials: SJ
authors.lastname: Machin
mesh_terms: D000328:Adult; D000368:Aged; D017304:Annexin A5 / Q000378:metabolism; D016736:Antiphospholipid Syndrome / Q000097:blood*; D001172:Arthritis, Rheumatoid / Q000097:blood; D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism / Q000502:physiology; D002449:Cell Aggregation; D015550:Cell Degranulation; D054641:Dual Specificity Phosphatase 2; D005260:Female; D006801:Humans; D007962:Leukocytes / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000097:blood*; D008297:Male; D008875:Middle Aged; D019007:P-Selectin / Q000097:blood; D015539:Platelet Activation / Q000187:drug effects; D010976:Platelet Count; D054648:Protein Phosphatase 2; D017027:Protein Tyrosine Phosphatases / Q000378:metabolism; D013927:Thrombosis / Q000097:blood; D014859:Warfarin / Q000494:pharmacology
chemical_list: D017304:Annexin A5; D019007:P-Selectin; D014859:Warfarin; D054648:Protein Phosphatase 2; C517032:DUSP2 protein, human; D054641:Dual Specificity Phosphatase 2; D017027:Protein Tyrosine Phosphatases; D001241:Aspirin