Studies of microparticles in patients with the antiphospholipid syndrome (APS)

Abstract

Objectives: To study circulating platelet, monocyte and endothelial microparticles (PMPs, MMPs and EMPs) in patients with antiphospholipid syndrome (APS) in comparison with healthy controls. Material and method: Fifty-two patients with APS and 52 healthy controls were investigated. MPs were measured on a flow cytometer (Beckman Gallios) and defined as particles sized < 1.0 mm, negative to phalloidin, positive to lactadherin and positive to either CD42a (PMPs), CD144 (EMPs) or CD14 (MMPs). Exposure of CD142 (TF) was measured on CD144 positive MPs. Results: Total number of MPs (i.e. lactadherin positive particles) was higher in APS patients versus controls (p < 0.001). An increased number of EMPs (p < 0.001), increased TF-positive EMPs (p < 0.001) and increased MMPs (p < 0.001) were also observed. PMP numbers did not differ between the groups. None of the MP types differed in numbers between obstetric and thrombotic APS patients. Conclusion: We observed a high number of EMPs expressing TF in APS patients. The numbers of MMPs and total EMPs were also higher as compared with healthy controls but in contrast to previous reports, the number of PMPs did not differ between groups. Lupus (2012) 21, 802-805.

Is a decrease of microparticles related to improvement of hemostasis after FVIII injection in hemophilia A patients treated on demand?

“…The samples were analyzed in a Beckman Coulter Gallios flow cytometer as previously described [15]. Briefly, the MP gate was determined using Megamix beads (0.5 lm, 0.9 lm and 3.0 lm; BioCytex, Marseille, France) ( , AH diagnostics, Stockholm, Sweden).…”

Modulating thrombotic diathesis in hereditary thrombophilia and antiphospholipid antibody syndrome: a role for circulating microparticles?

“…To date, there have been few studies targeting MPs in patients with APS or asymptomatic carriers of aPL and findings have been variable [75][76][77][78][79][80][81][82], mostly due to the small sample size and the heterogeneity of cases (primary/secondary APS, different aPL subtypes, presence/absence of obstetric complications) ( Table 2). Combes et al [75] pioneered the study of endothelial-MPs (CD51) in 30 patients with primary and secondary APS [only considering positivity for lupus anticoagulants (LAC)] and 30 healthy controls and found an approximately twofold increased of endothelial-MPs in the LAC patients; mean endothelial-MP levels were also higher in patients with thrombosis (n = 13).…”

“…However, they reported no differences in platelet-MPs in patients with APS and aPL+ compared with controls, although the levels were increased in APS with thrombotic complications compared with asymptomatic aPL. More recently, Vikerfors et al [79] measured endothelial-MPs (CD144), platelet-MPs (CD42a), monocyte-MPs (CD14), and endothelial-TF bearing MPs (CD144+/CD142+) in 52 patients with APS and 52 healthy controls. They showed increased numbers of endothelial-MPs, endothelial TFpositive MPs, and monocyte-MPs in APS compared with controls.…”

“…In conclusion, to date, findings on MPs in APS are conflicting and difficult to interpret, notably because patient numbers have mostly been small, patients included usually had aPL associated with SLE, and APS patients with obstetric complications were rarely studied. It is worth mentioning that four studies evaluated MPs levels in treated APS patients and the use of either anticoagulant (low-molecular-weight heparin or warfarin) or anti-platelet therapy did not affect MPs levels [75,77,79,80]. Summarizing, studies seem to confirm the following: (i) the presence of endothelial-MPs and platelet-MPs in APS and in asymptomatic carriers of aPL; (ii) the direct association of MPs with the presence of aPL (mainly anti-β 2 -glycoprotein) but not with underlying autoimmune disorders (mainly SLE) or the thrombotic event itself; (iii) no influence of anticoagulation therapy in MPs levels in APS.…”

Microparticles and their Roles in Inflammation: A Review§

“…Platelet-derived MPs associate with one of these aPLs, 2-glycoprotein-1 (apolipoprotein H) antibodies, implying a direct pathogenic role of platelet-derived MPs in APS [4]. Additionally, levels of TF-exposing endothelial cell-derived MPs are elevated in APS patients compared to healthy control group [55]. TF initiates the coagulation cascade via the extrinsic pathway and its upregulation mediated by aPLs has been established in APS [56].…”