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Pathogenesis of neuropsychiatric systemic lupus erythematosus and potential biomarkers
Modern Rheumatology, 07/29/09

Efthimiou P et al. – Review concludes that with continued advances in immunological research, new insights into the pathophysiologic mechanisms of neuropsychiatric systemic lupus erythematosus (NPSLE) may lead to the development of biomarkers and new treatment strategies.

Methods

Article reviews the recent literature pertaining to the pathogenesis of NPSLE
PUBMED database searches with no chronological constraints
Keywords: “neuropsychiatric systemic lupus erythematosus” cross-referenced with the terms “pathogenesis” and “biomarkers” for full-text articles in English

Results

Etiology of NPSLE is as yet unknown, though numerous autoantibodies and cytokines have been suggested as possible mediators
Autoantibodies and biomarkers elevated in nPSLE pts:
- Anti-phospholipid, anti-ribosomal P, anti-neuronal,
- Anti-glial fibrillary acidic protein (GFAP),
- Anti-endothelial cell, anti-N-methyl-d-aspartate (NMDA),
- Microtubule-associated protein 2 (MAP-2), and
- Matrix metalloproteinase-9 (MMP-9)
Cytokines that may be involved in the pathology of NPSLE include IL-2, IL-6, IL-8, IL-10, TNF-α and IFN-α and -γ

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