Background Patients with SLE have an increased risk of cardiovascular disease (CVD) and reasons for this are unknown. Microparticles (MPs) are membrane-bound particles released by many cells, 70–90% are derived from platelets. MPs are a rich source of autoantigens, including DNA and have many functions including thrombosis and inflammation. PMPs can induce foam cell formation and promote adherence of platelets to endothelial lesions. MPs are potentially important in the pathogenesis of autoimmune rheumatic disease and in cardiovascular disease.
Objectives To determine if EMPs and PMPs are increased in patients with SLE. Our secondary aim was to determine if there was a difference between those with/without subclinical cardiovascular disease and healthy controls.
Methods Atherosclerotic plaque was previously determined in patients with SLE who had no known history of CVD by carotid and femoral ultrasound scans. Plaque and thickened intima media thickness (IMT) >0.1cm were defined according to the Mannheim Carotid Consensus. Data regarding plaque area, IMT and echolucency were collected. Plasma was stored at -80° at the time of scan. Plasma from n=57; plaque (n=16), no plaque (n=23) and healthy controls (HC) (n=18) were analysed for presence of endothelial and platelet microparticles (EMPs and PMPs), as per protocol. Samples were stained with Annexin V and platelet and endothelial antibodies, CD42a, CD31, CD105 and CD144. MPs were measured using flow cytometry. Statistical analysis was carried out using PRISM.
Results A total of 57 plasma samples were tested. The average age of those with SLE was 45±12 years. 96% were female. 56% were Caucasian, 18% Asian, 21% Afrocaribbean, 5% other ethnicity. 18% of the SLE patients were smokers. Of the 18 HC, the average age was 37±7 years, 83% were female. 88% were Caucasian and 12% other ethnicity. 11% of the HCs were smokers. PMPs were significantly higher in patients with SLE compared to healthy controls (p=0.025). Patients with SLE without plaque had more PMPs compared to healthy controls (p=0.037). There was no correlation between age and PMPs. There was no statistical significance between those with SLE with plaque and healthy controls or in EMP levels between the three groups. There was no correlation between EMPs or PMPs with disease activity as measured by BILAG.
Conclusions PMPs were raised in patients with SLE compared to the healthy controls regardless of whether there was atherosclerotic plaque evident on imaging. Therefore, raised PMPs were associated with SLE itself and did not stratify a subset of patients with subclinical CVD. Further research is required to define whether PMP are important in the pathogenesis of SLE and to clarify the relationship of subclinical CVD in larger cohorts.
Disclosure of Interest None declared