Abstract
Cerebral and cardiovascular ischaemic events are frequent complications of SLE and constitute primary causes of permanent damage. However, the pathogenic determinants of an increased thromboembolic risk in patients with SLE are only partially understood. Atherosclerosis constitutes fertile soil for the development of thrombosis and shows disproportionately high prevalence and progression rates in patients with SLE. aPLs are independent risk factors for acute thrombosis but can also prompt long-term vascular inflammation. Aberrant interactions among immune cells and dysfunctions in the deployment of the coagulation cascade have historically been less explored in SLE, but recent evidence suggests they can also play a critical role at the crossroads between inflammation and haemostasis. In this review we discuss how different prothrombotic mechanisms can be prompted by and synergize with SLE-specific pathogenic events and speculate about novel potential directions for research and drug development.
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