Circulating microparticles in neuropsychiatric systemic lupus erythematosus

Phosphatidylserine-rich microparticles derived from endothelial cells, platelets and leukocytes have been implicated as surrogate markers of cellular activation in systemic lupus erythematosus (SLE). Because microparticles have also been associated with many primary neurologic diseases, this study investigated whether cellular-derived microparticles are also implicated in neuropsychiatric SLE (NPSLE).

Plasma microparticles were measured in 51 SLE patients and 22 age- and gender-matched controls. Acute NPSLE was defined as major NPSLE (acute stroke, transient ischemic attack, psychosis, isolated seizures, major cognitive disorder, or acute confusional state) and NPSLE disease activity was measured with the neurologic components of the SLE Disease Activity Index (Neuro-SLEDAI).

Neuro-SLEDAI levels varied widely in SLE patients, consistent with variable NPSLE activity. When considering all patients with SLE, there was no difference in total microparticles relative to matched controls, 2158/μL (interquartile range [IQR] 1214-3463) versus 2782/μL (IQR 1586-2990; P = 0.57) nor differences in microparticles derived from either platelets (P = 0.40), monocytes (P = 0.15) or endothelial cells (P = 0.32). However, levels of circulating monocyte-derived microparticles significantly and independently correlated with NPSLE (r = -0.28; P = 0.045), corticosteroid dosage (r = -0.38; P = 0.006) and levels of circulating C5a (r = 0.54; P < 0.0001). Non-neurologic SLE disease activity was not associated with microparticles.

Circulating cell-derived microparticles are reduced in active NPSLE, although the relative contribution of reduced microparticle production, increased consumption or intravascular sequestration, remain uncertain.