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Tissue Factor Pathway in Antiphospholipid Syndrome

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Hughes Syndrome

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Abstract

Thrombosis is the key lesion of the antiphospholipid syndrome (APS) [1,2]. Several non-exclusive mechanisms have been proposed to explain the involvement of antiphospholipid antibodies (aPL) in the pathogenesis of thrombosis in APS. These include inhibition of endothelial cell prostacyclin production [3–8], procoagulant effects on platelets [9, 10], impairment of fibrinolysis [11] and interference with the thrombomodulin-protein C-protein S pathway [12–14]. In addition, several studies have suggested that aPL can induce procoagulant activity (PCA) on vascular endothelial cells [9, 15, 16] and monocytes [10, 17–19].

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Authors
  1. P. M. Dobado-Berrios
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  2. C. López-Pedrera
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  3. F. Velasco
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  4. M. J. Cuadrado
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Editors and Affiliations

  1. Lupus Research Unit, St Thomas’ Hospital, Lambeth Palace Road, SE1 7EH, London, UK

    M. A. Khamashta MD, MRCP, PhD (Deputy Head) (Deputy Head)

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Dobado-Berrios, P.M., López-Pedrera, C., Velasco, F., Cuadrado, M.J. (2000). Tissue Factor Pathway in Antiphospholipid Syndrome. In: Khamashta, M.A. (eds) Hughes Syndrome. Springer, London. https://doi.org/10.1007/978-1-4471-3666-8_32

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  • DOI: https://doi.org/10.1007/978-1-4471-3666-8_32

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