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Platelet and endothelial activation are requisites for the development of antiphospholipid syndrome
  1. E del Río García1,
  2. C Rodríguez2,
  3. J Rodríguez-Martorell3,
  4. A Serrano1,
  5. J A Girón-González1
  1. 1Servicios de Medicina Interna, Hospital Universitario “Puerta del Mar”, Cádiz, Spain
  2. 2Inmunología, Hospital Universitario “Puerta del Mar”, Cádiz, Spain
  3. 3Hematología, Hospital Universitario “Puerta del Mar”, Cádiz, Spain
  1. Correspondence to:
    Dr J A Girón-González
    Servicio de Medicina Interna, Hospital Universitario “Puerta del Mar”, avda Ana de Viya 21, 11009, Cádiz, Spain; joseantonio.gironuca.es

https://doi.org/10.1136/ard.2003.010694

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    The antiphospholipid syndrome (APS) is characterised by venous and arterial thrombosis, recurrent fetal loss, and by the presence of antiphospholipid antibodies (aPL).1 aPL are also present in 2% of the healthy population,2,3 and, with the exception of those with high titres of aPL, there is no clear evidence of an increased incidence of thrombosis throughout the follow up.2–4 Thus, one of the key questions is: What causes the development of thrombosis in patients with APS? We suggest that in APS, a persistent procoagulant state,5,6 a continuous endothelial and platelet activation is present, and this may be detected by raised levels of soluble adhesion molecules.

    METHODS AND RESULTS

    We prospectively studied the following groups of subjects: (a) 20 patients …

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