Células endoteliales y micropartículas circulantes en pacientes portadores de anticuerpos antifosfolípidos / Circulating endothelial cells and microparticles in patients with antiphospholipid antibodies

Fundamento y objetivo: Determinar si los valores de células endoteliales circulantes (CEC), micropartículas circulantes (MP) y factor von Willebrand (FvW), marcadores establecidos de disfunción/daño endotelial, están elevados en pacientes portadores de anticuerpos antifosfolípidos (AAF) y si existe correlación con marcadores de inflamación y coagulación. Pacientes y método: Se estudian 12 pacientes portadores de AAF y 12 sujetos sanos. Se determinaron CEC, MP, FvW, proteína C reactiva (PCR), fibrinógeno (Fg), ácido siálico (AS), interleucina 6, factor tisular (FT), generación de trombina (GT) y fragmentos de protrombina (F1+2) y de fibrina (DD). Resultados: En los pacientes están significativamente elevados los valores de los marcadores de: disfunción/daño endotelial (CEC, MP y FvW), inflamación (Fg y PCR) y coagulación (FT y DD). El análisis bivariante muestra correlación significativa entre CEC y Fg, AS, PCR y DD, así como entre CEC y FvW y MP. Conclusión: Los pacientes portadores de AAF presentan una disfunción endotelial asociada a un proceso inflamatorio, que, unido a los valores elevados de Fg, FT y DD, puede inducir un estado de hipercoagulabilidad (AU)

Background and objective: To determine whether circulating endothelial cells (CECs), circulatingmicroparticles (MPs) and von Willebrand factor (vWF), established markers of endothelial dysfunction/ damage, are elevated in patients with antiphospholipid antibodies (aPL) and its possible correlation with inflammation and coagulation. Patients and methods: Twelve atients with aPL and 12 healthy subjects were studied. Levels of CECs, MPs, vWF, C reactive protein (CRP), fibrinogen (Fg), sialic acid (SA), interleukin 6 (IL-6), tissue factor (TF), thrombin generation (TG) and prothrombin (F1 + 2) and fibrin (DD) fragments were determined. Results: In patients, markers of dysfunction/damage endothelial, CECs, MPs and vWF; inflammation, Fgand CRP and coagulation, TF and DD were significantly elevated. The bivariate analysis showedsignificant correlation among CECs and Fg, AS, CRP and DD, as well as between CECs and vWF and MPs.Conclusion: Patients with aPL had endothelial dysfunction associated with an inflammatory process,which, together with high levels of Fg, TF and DD, may be responsible for the hypercoagulable state (AU)

[Circulating endothelial cells and microparticles in patients with antiphospholipid antibodies]. / Células endoteliales y micropartículas circulantes en pacientes portadores de anticuerpos antifosfolípidos.

BACKGROUND AND OBJECTIVE: To determine whether circulating endothelial cells (CECs), circulating microparticles (MPs) and von Willebrand factor (vWF), established markers of endothelial dysfunction/damage, are elevated in patients with antiphospholipid antibodies (aPL) and its possible correlation with inflammation and coagulation. PATIENTS AND METHODS: Twelve patients with aPL and 12 healthy subjects were studied. Levels of CECs, MPs, vWF, C reactive protein (CRP), fibrinogen (Fg), sialic acid (SA), interleukin 6 (IL-6), tissue factor (TF), thrombin generation (TG) and prothrombin (F1+2) and fibrin (DD) fragments were determined. RESULTS: In patients, markers of dysfunction/damage endothelial, CECs, MPs and vWF; inflammation, Fg and CRP and coagulation, TF and DD were significantly elevated. The bivariate analysis showed significant correlation among CECs and Fg, AS, CRP and DD, as well as between CECs and vWF and MPs. CONCLUSION: Patients with aPL had endothelial dysfunction associated with an inflammatory process, which, together with high levels of Fg, TF and DD, may be responsible for the hypercoagulable state.

Yasmin and venous thromboembolism: new case reports.

It is not yet known whether Yasmin involves a higher thrombotic risk compared with other contraceptives. We present a serie of eight new cases of women who developed thrombotic events early after starting on Yasmin who were sent to our Thrombosis and Hemostasis Unit for a thrombophilia work-up in the last five years. Only two of them were heterozygous carriers of the prothrombin G20210A mutation and three were obese while none of them were smoker. These new cases provide information about the characteristics of the thrombotic events and the concomitant risk factors, indicating that this pill may not be as safe as had been previously thought, and suggest that new studies regarding safety profile of Yasmin are required to explain the association with venous thrombotic events.

Haemorheological alterations in Behçet's disease are not related to a tendency for venous thrombosis.

INTRODUCTION: Behçet's disease is associated with an increased risk of thrombosis, although the prothrombotic mechanisms are unclear. Alterations in blood rheology, particularly increased erythrocyte aggregation, might play a role in the development of such thrombotic events. MATERIALS AND METHODS: We measured plasma lipids, fibrinogen, haematocrit, erythrocite aggregation, erythrocyte deformability, blood viscosity, plasma viscosity and erythrocyte indexes in patients with a nonactive disease at sampling, and in a well-matched control group. The patient group comprised 42 patients with BD (21 male, 21 female aged 43+/-12 years) and the control group comprised 46 healthy volunteers (23 male, 23 female aged 45+/-13 years). Twelve of the 42 patients with BD had a previous documented history of deep vein thrombosis at least 6 months before entering the study, and the other 30 did not. RESULTS: Compared with controls, patients showed statistically higher fibrinogen concentrations (P=0.001), plasma viscosity (P=0.002), blood viscosity (P=0.006) and erythrocyte aggregation, both at stasis (P=0.001) and at a low shear rate (P=0.002): the other rheological parameters were not statistically significant. No differences were observed in the rheological parameters when patients with and without previous thrombotic episodes were compared. CONCLUSIONS: Although patients with BD show a moderate hyperviscosity syndrome, possibly related to chronic inflammation, this does not seem to play a role in the development of thrombotic events.

Influence of plasma and erythrocyte factors on red blood cell aggregation in survivors of acute myocardial infarction.

Increased erythrocyte aggregation (EA) has been observed in patients with ischaemic heart disease (IHD), although most of these studies have been performed in the acute phase when reactant proteins may account for this increase. Little is known about the role played by the erythrocyte itself in this aggregation process. To ascertain the contribution of both plasma and erythrocyte factors to EA in IHD, we investigated the following parameters in 78 survivors of acute myocardial infarction (AMI) and in a well-matched control group of 98 subjects: EA, glucose, total cholesterol (T-Chol), low-density lipoprotein-cholesterol (LDL-Chol), high-density lipoprotein-cholesterol (HDL-Chol), triglycerides, apolipoproteins A(1) and B, protein and functional fibrinogen, plasma sialic acid, membrane sialic acid, and the cholesterol and phospholipid content of the erythrocyte membrane. AMI survivors showed higher glucose (p<0.001), a borderline increase in triglycerides (p = 0.043), and a statistical decrease in Apo A(1) (p= 0.003) relative to controls. EA, functional fibrinogen, and plasma sialic acid were statistically higher in AMI survivors than in controls (p= 0.001; p<0.001; p= 0.011, respectively). Membrane sialic acid content was statistically lower in AMI patients than in controls (p= 0.026). No differences were observed in either membrane cholesterol or phospholipids. Multivariate logistic regression analysis, in which EA was dichotomized as higher or lower than 8.7, demonstrated that triglyceride levels higher than 175 mg/dL (OR= 7.7, p= 0.001) and functional fibrinogen levels higher than 320 mg/dL (OR= 3.7, p= 0.004) were independently associated with a greater risk of erythrocyte hyperaggregability. Our results suggest that plasma lipids, predominantly triglycerides, and fibrinogen may not only enhance the development of ischaemic events by their recognized atherogenic mechanisms, but also by increasing EA.