Journal
CLINICAL IMMUNOLOGY
Volume 228, Issue -, Pages -Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2021.108755
Keywords
Systemic lupus erythematosus; Cardiovascular disease; Thrombosis; Antiphospholipid syndrome; Complement split products; Platelet; Inflammation; Autoimmune disease; Biomarker
Categories
Funding
- YG - National Center for Advancing Translational Sciences at the National Institutes of Health [TL1 TR001875]
- American Philosophical Society Daland Fellowship
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Elevated levels of PC4d are associated with arterial events in SLE patients, independent of antiphospholipid status, smoking, and prednisone use. PC4d levels are correlated with abnormalities in platelet function and may serve as a mechanistic marker for vascular disease in SLE.
Platelet-bound complement activation products (PC4d) are associated with thrombosis in Systemic Lupus Erythematosus (SLE). This study investigated the effect of PC4d on platelet function, as a mechanistic link to arterial thrombosis. In a cohort of 150 SLE patients, 13 events had occurred within five years of enrollment. Patients with arterial events had higher PC4d levels (13.6 [4.4-24.0] vs. 4.0 [2.5-8.3] net MFI), with PC4d 10 being the optimal cutoff for event detection. The association of arterial events with PC4d remained significant after adjusting for antiphospholipid status, smoking, and prednisone use (p = 0.045). PC4d levels correlated with lower platelet counts (r = -0.26, p = 0.002), larger platelet volumes (r = 0.22, p = 0.009) and increased platelet aggregation: the adenosine diphosphate (ADP) concentration to achieve 50% maximal aggregation (EC50) was lower in patients with PC4d 10 compared with PC4d < 10 (1.6 vs. 3.7, p = 0.038, respectively). These results suggest that PC4d may be a mechanistic marker for vascular disease in SLE.
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