Epidemiology of premature vascular damage in systemic lupus erythematosus

systemic lupus erythematosus Systemic lupus erythematosus (SLE) is an autoimmune disease with heterogeneous manifestations, including internal organ damage, which can result in severe morbidity and even death and often requires aggressive immunosuppressive treatment. More than 30 years ago, a bimodal peak in mortality was described in lupus patients, with late increases in death commonly seen as secondary to premature cardiovascular disease (CVD) [1]. Indeed, this enhanced atherosclerotic risk increases with each year of disease duration. Th is is especially the case in young females with SLE, where the CVD risk can be up to 50-fold higher than in age-matched controls [2,3]. While traditional Framingham risk factors likely contri bute to CVD in SLE, they cannot fully account for the increased risk. Instead, the pathogenesis of premature CVD in SLE may rely on factors unique to the disease itself [4]. While systemic infl ammation has been linked to atherosclerosis development in the general population and in specifi c conditions, SLE typically has a lower ‘classical infl ammatory burden’ compared to what would be seen in rheumatoid arthritis or spondylo arthropathies; yet, lupus is associated with a higher CVD risk than these other diseases. Th is observation suggests that factors that trigger accelerated atherosclerosis in lupus diff er from the typical proinfl ammatory factors (that is, high C-reactive protein (CRP)) linked to ‘idiopathic’ athero sclerosis. Atherosclerosis progression in lupus patients develops or progresses in 10% of SLE patients per year. Among other factors, this progression is associated with older age at diagnosis and with longer disease duration, supporting the hypothesis that chronic exposure to lupus immune dysregulation promotes CVD [5].