Key result
Proinflammatory high-density lipoproteins, found in 45% of patients with systemic lupus erythematosus and 20% with rheumatoid arthritis, contribute to accelerated atherosclerosis.
This review highlights the role of proinflammatory HDLs in driving accelerated atherosclerosis in patients with chronic rheumatic diseases like SLE and RA.
HDL phenotyping not ready for clinical use in SLE or RA; leaves open whether targeting proinflammatory HDL improves outcomes.
In this review, the authors discuss the formation and structure of high-density lipoproteins (HDLs) and how those particles are altered in inflammatory or stress states to lose their capacity for reverse cholesterol transport and for antioxidant activity. In addition, abnormal HDLs can become proinflammatory (piHDLs) and actually contribute to oxidative damage. The assay by which piHDLs are identified involves studying the ability of test HDLs to prevent oxidation of low-density lipoproteins. Finally, the authors discuss the potential role of piHDLs (found in some 45% of patients with systemic lupus erythematosus and 20% of patients with rheumatoid arthritis) in the accelerated atherosclerosis associated with some chronic rheumatic diseases.
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Hahn et al. (2008) conducted a review in Systemic lupus erythematosus and rheumatoid arthritis. Proinflammatory high-density lipoproteins was evaluated. Proinflammatory high-density lipoproteins, found in 45% of patients with systemic lupus erythematosus and 20% with rheumatoid arthritis, contribute to accelerated atherosclerosis.
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