WASHINGTON, D.C.—Experts at the 2016 ACR/ARHP Annual Meeting session, Systemic Lupus Erythematosus—Clinical Aspects and Treatment IV: Biomarkers, reported on a number of recent studies showing advancement in our understanding of the disease mechanisms underlying systemic lupus erythematosus (SLE) that place these patients at risk for cardiovascular disease (CVD) and other comorbidities.
Mechanisms of CVD Risk in SLE Patients
Among the presentations on mechanisms of CVD risk in SLE patients was one by Monica Purmalek, a first-year medical student in the Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Md., who reported on the results of a cross-sectional study that tested the hypothesis that aberrant neutrophil subsets contribute significantly to vascular damage and unstable plaque development in patients with SLE.
The study was done to more comprehensively characterize CVD in SLE patients given that CVD is a leading cause of mortality in CVD, said Ms. Purmalek. Specifically, investigators were interested in “identifying whether immune dysregulation and innate immune responses associated with aberrant neutrophils play a key role in driving vascular damage,” she said.
To test this hypothesis, investigators collected clinical and demographic characteristics, Framingham Risk scores, metabolic parameters and lupus medications on a cohort of 54 SLE patients and 32 healthy controls matched by age and gender. In this cohort, they assessed the vascular function of various arterial territories, aortic inflammation by positron emission tomography (PET), with fluorodeoxyglucose (FDG), and computed tomography (CT), and anatomical assessment of plaque by coronary CT angiogram. Flow cytometry was used to quantify circulating low-density granulocytes.
The study found that, compared with the healthy controls, SLE patients had significant impairments in endothelial function and enhanced arterial stiffness suggestive of widespread inflammation and damage across both micro- and macrovascular territories.
“Our results support the hypothesis that aberrant neutrophil subsets significantly contribute to vascular damage and unstable plaque development in patients with SLE,” said Ms. Purmalek. “Our findings suggest that neutrophils, through neutrophil extracellular trap formation, may disrupt [high-density lipoprotein] HDL function and further promote atherogenesis.”
Biomarkers for Cardiovascular Disease in SLE
In another presentation that looked at biomarkers for cardiovascular disease in SLE patients, Ashira Blazer, MD, a rheumatologist at The New York University School of Medicine, N.Y., reported the results of a study that focused on genetic variants in African Americans that place SLE patients at increased risk of developing CVD. These genetic variants are two apolipoprotein L1 (APOL1) risk variants, G1 and G2, located on chromosome 22q12.3 that show a link to excess renal risk in African Americans.
