Alonso, A. (Andrés)

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    Reseñas 39/1 (2006)
    (2006) Carbonell, C. (Claudia); Ruiz-Danneger, C. (Constanza); Sánchez-León, A. (Alberto); Ortiz-de-Landázuri, C. (Carlos); Serantes, A. (Arantxa); Alonso, A. (Andrés); Ghiretti, H. (Héctor); Pereda, R. (Rubén); Hierrezuelo, G. (Guillermo); Runnquist, E. (Elin); Crespo, M. (Mariano)
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    DERRIDA, J., Canallas. Dos ensayos sobre la razón, Trotta, Madrid, 2005. [RECENSIÓN]
    (Servicio de Publicaciones de la Universidad de Navarra, 2006) Alonso, A. (Andrés)
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    Autoantibodies against the endothelial receptor of protein C are associated with acute myocardial infarction in young women
    (Wiley-Blackwell, 2005) Foco, L. (L.); Hermida, J. (José); Alonso, A. (Andrés); Zonzin, P. (P.); Hurtado, V. (Verónica); Montes, R. (Ramón); Mannucci, P.M. (P.M.)
    BACKGROUND: Acute myocardial infarction (AMI) is rare among young women. The search for unknown risk factors is warranted. Endothelial protein C receptor (EPCR) is largely present at the endothelial surface of large arteries. No studies about association of anti-EPCR autoantibodies (anti-EPCR) with AMI are available. METHODS: Plasma IgA, IgM and IgG anti-EPCR levels were measured by enzyme-linked immunosorbent assay in 165 women younger than 45 years who survived a first AMI and 165 healthy women, matched by age and geographical origin. RESULTS: Using the 90th percentile of IgA anti-EPCR in the control group, IgA anti-EPCR were independently associated with AMI after adjustment for cardiovascular risk factors (OR 5.1; 95% CI 1.7-15.6; P = 0.004). The risk apparently conferred by IgA anti-EPCR increased dose-dependently (P for trend =0.0002). IgM anti-EPCR were less consistently associated with AMI: a significant increase in the risk was found when women above the 90th percentile were compared with those in the lowest quartile (OR 3.6; 95% CI 1.2-11.5; P = 0.03). IgG anti-EPCR were similar in patients and controls. A total of 145 patients underwent coronary arteriography. IgA or IgM anti-EPCR were not different among patients with different degrees of atherosclerotic lesion (anova, P = 0.77 and 0.24, respectively). CONCLUSIONS: High levels of IgA and, to a lesser extent, IgM anti-EPCR, are associated with AMI in young women.
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    Association of increased fibrinogen concentration with impaired activation of anticoagulant protein C
    (Wiley-Blackwell, 2006) Hermida, J. (José); Alonso, A. (Andrés); Navarro, S. (Silvia); Diez-Goñi, N. (Nieves); España, F. (Francisco); Montes, R. (Ramón); Medina, P. (Pilar)
    BACKGROUND: Low levels of activated protein C (APC) are a risk factor for venous thrombosis. The mechanisms leading to interindividual differences in APC are not totally elucidated. Protein C is activated by the thrombin-thrombomodulin complex. As thrombin binds to fibrinogen and thrombomodulin through a common region, it is conceivable that fibrinogen influences the activation of protein C. This would help to explain the association between high levels of fibrinogen and an increased thrombotic risk. METHODS: We analyzed the association between circulating APC levels and fibrinogen concentration in 382 healthy subjects. Subsequently, we studied the effect of increasing fibrinogen concentrations on the APC generation on cultured endothelial cells. RESULTS: An independent inverse association between circulating APC levels and fibrinogen was found [betacoefficient, -0.16; 95% confidence interval (95% CI) -0.26, -0.06; P = 0.001]. For each 100 mg dL(-1) increase in fibrinogen, the independent risk of having low APC levels (<0.7 ng mL(-1)) was almost three times higher (OR 2.8; 95% CI 1.1, 7.2; P = 0.04). Accordingly, a notable association between increasing fibrinogen concentrations and the reduction in the thrombin-thrombomodulin dependent activation of protein C on endothelial cells was found (r = -0.57; P = 0.002). CONCLUSIONS: We present evidence of an inverse association between circulating APC and fibrinogen levels. According to this finding together with the results of our in vitro experiments, we propose that the impairment in the generation of APC on endothelial cells constitutes a new prothrombotic mechanism of fibrinogen.