Golovach I.Yu.1, Yehudina Ye.D.2, Ter-Vartanіan S.Kh.2

Summary. Neuropsychiatric systemic lupus erythematosus (NPSLE) is characterized by damage to both the central and peripheral nervous systems, and is the second leading cause of mortality and morbidity in patients with systemic lupus erythematosus (SLE) after lupus nephritis. Diagnosis and treatment of NPSLE remains a challenge, since the pathogenesis of this condition has not been fully understood. The purpose of the study: to study data on modern advances in diagnostic methods, pathogenetic mediators and potential treatment methods for NPSLE. Materials and methods. This paper presents a review of the literature on the diagnosis, pathogenesis and treatment of NPSLE, based on a search of English-language articles in the Medline and PubMed databases published from January 2017 to June 2019. Results and discussion. Screening tools for neurodegenerative diseases have been found to be sensitive and specific for the assessment of cognitive dysfunction in NPSLE. Neuroimaging can be used to diagnose patients with SLE compared with the control group of healthy people, but further research is needed to differentiate SLE with and without neuropsychiatric manifestations. Elevated levels of certain molecules in the cerebrospinal fluid and/or serum, as well as the presence of certain autoantibodies, have been identified as potential NPSLE biomarkers. Among them, anti-NR2 and anti-ribosomal P autoantibodies, lipocalin 2 and osteopontin, these markers have not only pathogenetic, but also diagnostic value. Studies show that damage to the blood-brain barrier does not always play a role in the development of NPSLE, as previously thought. There is new evi­dence of a decrease in the severity of the disease after microglia modulation, suggesting direct damage to the central nervous system, as a leading mechanism in the NPSLE pathogenesis. Conclusions. NPSLE include various symptoms that affect the quality of life and prognosis of the patient. Recently, successes have been achieved in improving the diagnosis of NPSLE, as well as in understanding pathogenesis. New variants of targeted therapy are presented, based on a clearer understanding of the pathogenesis of NPSLE, which show an improvement in the course of NPSLE in mouse models. Further evaluation of these treatments is needed in patients with NPSLE, as well as the potential use of neuroimaging to distinguish patients with SLE with or without neuropsychiatric manifestations.

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