Lupus & antiphospholipid syndrome
A Multiomic Analysis to Identify Drivers of Subclinical Vascular Disease in Systemic Lupus Erythematosus
Authors' conclusion
Blood gene expression patterns and serum proteins that associate with worse vascular phenotypes suggest dysregulated immune and metabolic pathways linked to premature CVD.
Study context
- Population
- Patients with systemic lupus erythematosus (SLE) and healthy controls assessed for arterial stiffness (cardio-ankle vascular index (CAVI)), vascular wall inflammation (FDG-PET/CT TBR) and coronary atherosclerosis burden (coronary CT angiography)
- Participants
- 77 vs 27
- Exposure
- SLE vs healthy controls
- SLEn = 77
- Healthy controls (HCs)n = 27reference
- Outcome
- Subclinical vascular disease: CAVI, TBR and noncalcified coronary plaque burden (NCB)
Methodological detailsmultiomic, whole blood bulk RNA sequencing, Olink serum protein biomarkers
- Multiomic
- Whole blood bulk RNA sequencing
- Olink serum protein biomarkers
Main finding
As reported in the abstract
- Serum proteins associated with increased CAVI: CCL23, CSF-1, LAP TGF-β1, IL-33, CD8A, IL-12B
- P < 0.05
- Serum proteins associated with NCB: MCP-4, Flt3L
- P < 0.05
- Serum proteins associated with TBR: CD5, IL-1α, AXIN1, CST5, TNFRSF9
- P < 0.05
Observational data: associations, not effects.
Original publication
A Multiomic Analysis to Identify Drivers of Subclinical Vascular Disease in Systemic Lupus Erythematosus. Arthritis Rheumatol. Published 15 July 2024. doi:10.
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