Abstract
Systemic lupus erythematosus is a classical systemic autoimmune disease that overactivates complement and can affect all organs. Early diagnosis and effective management are important in this immune-complex-mediated chronic inflammatory disease, which has a strong component of vasculitis and carries an increased risk of thrombosis, even in the absence of antiphospholipid antibodies. Development of lupus nephritis can be life limiting but is managed with dialysis and renal transplantation. Therefore, data have become available that cardiovascular risk poses a serious feature of systemic lupus erythematosus that requires monitoring and prospective treatment. Cell-derived microparticles circulate in plasma and thereby intersect the humoral and cellular component of inflammation. They are involved in disease pathophysiology, particularly thrombosis, and represent a known cardiovascular risk. This viewpoint argues that a focus on characteristics of circulating microparticles measured in patients with systemic lupus erythematosus may help to classify certain ethnic groups who are especially at additional risk of experiencing cardiovascular complications.
Highlights
Systemic lupus erythematosus (SLE) is an immune-complex-driven disease which engages complement activation via recognition of circulating and bound immune complexes by the classical pathway
An indifferent outcome of the extent of complement activation in relation to tissue damage was reported in patients with SLE [12] but immunoglobulin binding subsets of microparticles, which fix complement, are more likely to follow disease activity [13]
Platelet-derived microparticles generate thrombin, thereby aggravating hypercoagulability. Circulating microparticles, including those derived from endothelial cells, are novel biomarkers in SLE [17], but studies have not related these to clinical disease activity [3,18,19,20] or evaluated for cardiovascular risk in SLE the proportion of IgG-decorated microparticles that fixed complement [21]
Summary
Systemic lupus erythematosus (SLE) is an immune-complex-driven disease which engages complement activation via recognition of circulating and bound immune complexes by the classical pathway. Microparticles are released from activated, apoptotic or dying cells by a process called blebbing whereby membrane remodelling modification and phosphatidylserine exposure result in an extrusion incorporating parental surface proteins and contents [4]. An indifferent outcome of the extent of complement activation in relation to tissue damage was reported in patients with SLE [12] but immunoglobulin binding subsets of microparticles, which fix complement, are more likely to follow disease activity [13]. Their association with cardiovascular risk in patients with SLE has not yet been studied. A need for studies that stratify severity to novel biomarkers has recently been identified [14]
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