“…This process is associated with increased expression of luminal adhesion molecules (eg, vascular cell adhesion molecule 1 (VCAM-1)), leukocyte recruitment and disassembly of cell–cell junctions, finally resulting in loss of barrier function and tissue oedema 5. In SLE, several lines of evidence demonstrate excessive endothelial activation in response to immune complexes, anti-endothelial cell antibodies, anti-double-stranded DNA (dsDNA) antibodies, various cytokines (eg, tumour necrosis factor (TNF)α) and anti-phospholipid antibodies 6 7 8 9 10…”