The pathophysiology of the antiphospholipid syndrome (APS) is multifaceted, complex, and as yet incompletely understood. Of central importance are pathogenic antiphospholipid antibodies (aPLs) which affect several cell types, including platelets, monocytes, trophoblastic, decidual, and endothelial cells as well as components of the coagulation and fibrinolytic systems. The result of these actions is an increased tendency towards arterial and venous thrombosis and atherosclerotic cardiovascular disease, especially when associated with inflammation and oxidative stress. The functional and molecular properties of aPL are potentially important markers in predicting clinical outcomes in APS patients. These properties of aPL could be especially useful in predicting the outcome when coupled with genomic and proteomic biomarkers of clinical events in APS. This chapter highlights the current evidence relating to the various pathophysiological mechanisms important in APS and potential biomarkers related to clinical outcomes.
CITATION STYLE
Willis, R., Giles, I. P., Chen, P. P., López-Pedrera, C., Cuadrado, M. J., & Pierangeli, S. S. (2012). What is the mechanism(S) of antiphospholipid antibody-mediated thrombosis? In Antiphospholipid Syndrome: Insights and Highlights from the 13Th International Congress on Antiphospholipid Antibodies (pp. 57–78). Springer US. https://doi.org/10.1007/978-1-4614-3194-7_4
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