Accelerated atherosclerosis in systemic lupus erythematosus
Authors:
A. Smržová; P. Horák; M. Skácelová; H. Ciferská
Authors‘ workplace:
III. interní klinika FN a LF UP Olomouc
Published in:
Čes. Revmatol., 17, 2009, No. 3, p. 173-178.
Category:
Overview Reports
Overview
Accelerated atherosclerosis (ATS) in connective tissue diseases is a very serious late disease-related complication. In systemic lupus erythematosus (SLE), the risk of ATS is sevenfold increased in comparison to an age-matched healthy population, and comparable to Cushing’s syndrome (e.g. more than threefold increased in comparison to diabetes mellitus). It is therefore important to pay attention to primary, as well as secondary prevention. An inflammatory process involving the vascular wall, presence of some specific antibodies, dyslipidemia, endothelial dysfunction, and an increased appearance of traditional risk factors play a significant role in the pathophysiology of ATS. The existence of these factors has various causes; they result from the autoimmune character of SLE, with participation of the used therapy. High cumulative doses of glucocorticoids, and cyclosporin A have a negative effect on ATS, whereas antimalarial drugs, mycophenolate mofetil, or some new biological agents have a protective effect. Accelerated atherosclerosis in SLE is a very complex and complicated process, and deserves sufficient attention, especially since the consequences of ATS significantly participate in the morbidity and mortality of SLE.
Key words:
accelerated atherosclerosis, systemic lupus erythematosus, dyslipidemia, glucocorticoids, cyclosporin A, antimalarial drugs
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