Sander Deijns, Netherlands

UMC Utrecht Rheumatology and clinical immunology
I am an elderly care physician in training, currently working in a nursing home in Nieuwegein (the Netherlands). I work with geriatric patients with both physical and cognitive disabilities. As you might notice, I am not an expert in this particular field. During my study in medicine, I did my research internship at the rheumatology and clinical immunology ward at the UMC Utrecht hospital. I conducted a narrative review on the pathophysiology of psychiatric manifestations attributed to SLE. By reading al lot of articles, I was able to construct a new potential pathophysiologic model for these manifestations.

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THE IMMUNOLOGIC ETIOLOGY OF PSYCHIATRIC MANIFESTATIONS IN SYSTEMIC LUPUS ERYTHEMATOSUS: A NARRATIVE REVIEW ON THE ROLE OF THE BLOOD BRAIN BARRIER, ANTIBODIES, CYTOKINES AND CHEMOKINES

Session Name
PS50 - THE INVOLVEMENT OF AUTOIMMUNITY IN CNS
Session Type
PARALLEL SESSIONS
Date
31.05.2021, Monday
Session Time
13:30 - 15:30
Room
HALL D
Lecture Time
14:00 - 14:10
Presenter
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Abstract

Background and Aims

The aim of this narrative review is to provide an overview of the literature on the possible immunologic pathophysiology of psychiatric manifestations of neuropsychiatric systemic lupus erythematosus (NPSLE).

Methods

A systematic search on PubMed was conducted. English studies with full text availability that investigated the correlation between blood-brain barrier (BBB) dysfunction, intrathecal synthesis of antibodies, antibodies, cytokines, chemokines, metalloproteinases, complement and psychiatric NPSLE manifestations in adults were included.

Results

Both transient BBB-dysfunction with consequent access of antibodies to the cerebrospinal fluid (CSF) and intrathecal synthesis of antibodies could occur in psychiatric NPSLE. Anti-phospholipid antibodies, anti-NMDA antibodies and anti-ribosomal protein p antibodies seem to mediate concentration dependent neuronal dysfunction. Interferon-α may induce microglial engulfment of neurons, direct neuronal damage and production of cytokines and chemokines in psychiatric NPSLE. Several cytokines, chemokines and matrix metalloproteinase-9 may contribute to the pathophysiology of psychiatric NPSLE by attracting and activating Th1-cells and B-cells.

Conclusions

This potential pathophysiology may help understand NPSLE and may have implications for the diagnostic management and therapy of psychiatric NPSLE. However, the presented pathophysiological model is based on correlations between potential immunologic etiologies and psychiatric NPSLE that remain questionable. More research on this topic is necessary to further elucidate the pathophysiology of NPSLE.

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