Stroke and Systemic Lupus Erythematosus: A Review

Abstract

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that involves collagen tissue throughout the body. Several previous studies have shown that the risk of ischaemic and haemorrhagic stroke is significantly higher in SLE when compared to the general population, particularly in young individuals, representing one of the principal causes of death in these patients. Though the precise pathophysiology behind this increased risk is still poorly understood, several mechanisms are suggested to play a role. The high burden of cerebral small vessel disease features noted on brain neuroimaging studies, as well as the accelerated process of atherosclerosis identified in these patients, are likely to be responsible for at least some of the ischaemic strokes occurring in the SLE population. Repeated episodes of arterial and venous thrombosis secondary to antiphospholipid syndrome are likewise important. Less is known regarding the exact pathophysiological relationship between SLE and the high incidence of haemorrhagic stroke, though thrombocytopenia and a greater susceptibility to form typical and atypical brain aneurysms, which may then rupture, are thought to be the main mechanisms responsible for the occurrence of intracerebral and subarachnoid haemorrhage, respectively. Both inflammatory and noninflammatory events, all involving the immune system, are responsible for several pathological changes affecting cerebral vessels of every calibre in SLE, as confirmed by histopathology. In this context, endothelial activation and dysfunction play a critical role. This review will briefly analyse the most important factors responsible for the higher ischaemic and haemorrhagic stroke risk in the SLE population, with a particular focus on brain vascular changes.