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Review
. 2021 Mar 1;33(2):211-218.
doi: 10.1097/BOR.0000000000000773.

The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy

Affiliations
Review

The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy

Brenna D Appleton et al. Curr Opin Rheumatol. .

Abstract

Purpose of review: Accelerated atherosclerosis is a significant comorbidity and the leading cause of death for patients with systemic lupus erythematosus (SLE). It is now apparent that SLE-accelerated atherosclerosis is not driven solely by traditional cardiovascular risk factors, adding complexity to disease characterization and mechanistic understanding. In this review, we will summarize new insights into SLE-accelerated atherosclerosis evaluation, treatment, and mechanism.

Recent findings: Recent work highlights the need to incorporate inflammatory biomarkers into cardiovascular disease (CVD) risk assessments. This is especially true for SLE patients, in which mechanisms of immune dysfunction likely drive CVD progression. There is new evidence that commonly prescribed SLE therapeutics hinder atherosclerosis development. This effect is achieved both by reducing SLE-associated inflammation and by directly improving measures of atherosclerosis, emphasizing the interconnected mechanisms of the two conditions.

Summary: SLE-accelerated atherosclerosis is most likely the consequence of chronic autoimmune inflammation. Therefore, diligent management of atherosclerosis requires assessment of SLE disease activity as well as traditional cardiovascular risk factors. This supports why many of the therapeutics classically used to control SLE also modulate atherosclerosis development. Greater understanding of the mechanisms underlying this condition will allow for the development of more targeted therapeutics and improved outcomes for SLE patients.

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Conflict of interest statement

Conflicts of Interest

There are no conflicts of interest.

References

    1. Ward MM, Pyun E, Studenski S. Causes of death in systemic lupus erythematosus. Long-term followup of an inception cohort. Arthritis Rheum. 1995. October;38(10):1492–9. - PubMed
    1. Urowitz MB, Gladman DD, Tom BDM, et al. Changing patterns in mortality and disease outcomes for patients with systemic lupus erythematosus. J Rheumatol. 2008;35(11):2152–8. - PubMed
    1. Thomas G, Mancini J, Jourde-Chiche N, Sarlon G, et al. Mortality associated with systemic lupus erythematosus in France assessed by multiple-cause-of-death analysis. Arthritis Rheumatol. 2014;66(9):2503–11. - PubMed
    1. Bartels CM, Buhr KA, Goldberg JW, et al. Mortality and cardiovascular burden of systemic lupus erythematosus in a US population-based cohort. J Rheumatol. 2014;41(4):680–7. - PMC - PubMed
    1. Urowitz MB, Gladman D, Ibañez D, et al. Clinical manifestations and coronary artery disease risk factors at diagnosis of systemic lupus erythematosus: Data from an international inception cohort. Lupus. 2007;16(9):731–5. - PubMed

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