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Circulating microparticles in neuropsychiatric systemic lupus erythematosus

Authors

  • Kendall P. Crookston,

    Corresponding author
    1. Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico, USA
    • Department of Pathology, University of New Mexico School of Medicine, Albuquerque, New Mexico, USA
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  • Wilmer L. Sibbitt Jr.,

    1. Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico, USA
    2. Department of Neurology, University of New Mexico School of Medicine, Albuquerque, New Mexico, USA
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  • Wayne. L. Chandler,

    1. Department of Pathology and Genomic Medicine, The Methodist Hospital, Houston, Texas, USA
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  • Clifford R. Qualls,

    1. Department of Mathematics and Statistics, University of New Mexico, Albuquerque, New Mexico, USA
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  • Carlos A. Roldan

    1. Department of Internal Medicine, University of New Mexico School of Medicine, Albuquerque, New Mexico, USA
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  • All authors contributed equally to the study design and manuscript preparation.

Correspondence: Kendall P. Crookston, University of New Mexico School of Medicine, MSC08-4640, 1 University of New Mexico, Albuquerque, NM 87131, USA.

Email: kcrookston@salud.unm.edu

Abstract

Aim

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).

Method

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).

Results

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; < 0.0001). Non-neurologic SLE disease activity was not associated with microparticles.

Conclusion

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

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