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Inflammatory markers and indicators of systemic endotoxemia in patients with treatment-resistant schizophrenia

INTRODUCTION: Elevated levels of lipopolysaccharide (LPS) in circulation support chronic inflammation, which is involved in the pathological process in the brain and may be a contributing factor to treatment resistance in schizophrenia. OBJECTIVES: To compare inflammatory markers and indicators of s...

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Detalles Bibliográficos
Autores principales: Zozulya, S. A., Otman, I. N., Anikhovskaya, I. A., Tikhonov, D. V., Kaleda, V. G., Yakovlev, M. Y., Klyushnik, T. P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cambridge University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10595862/
http://dx.doi.org/10.1192/j.eurpsy.2023.568
Descripción
Sumario:INTRODUCTION: Elevated levels of lipopolysaccharide (LPS) in circulation support chronic inflammation, which is involved in the pathological process in the brain and may be a contributing factor to treatment resistance in schizophrenia. OBJECTIVES: To compare inflammatory markers and indicators of systemic endotoxemia (SE) in patients with treatment-resistant schizophrenia and in those with a good response to treatment. METHODS: The study involved 34 patients with schizophrenia (27±7,5 years) (F20) in an acute psychotic state: 15 patients with TRS (non-responders), 19 patients responded to treatment with reduced symptoms (responders). The markers of systemic inflammation (leukocyte elastase (LE) and a1-proteinase inhibitor (α1-PI) activity, CRP concentration, antibodies (Abs) to S100B and myelin basic protein) and the indicators of SE (LPS level and Abs to LPS) were determined in the blood of patients. RESULTS: The responders showed a significant increase in LE and α1-P1 activity (p<0.001), CRP concentration (p<0.05), and Abs to neuroantigens (p<0.05) compared to controls. LPS levels did not differ from control values. In non-responders, a moderate increase in LE and α1-PI activities (p<0.05) and a significant increase in CRP concentration (p=0.01) were accompanied by no significant differences in Abs to neuroantigens. These patients had elevated LPS level and Abs to LPS deficiency compared with both responders (p<0.01) and controls (p<0.05). CONCLUSIONS: The identified spectra of systemic inflammation markers, elevated LPS level, and insufficient anti-endotoxin immunity in patients with treatment-resistant schizophrenia may be related to endotoxin tolerance. Further research in this field can help develop new approaches to overcoming resistance to therapy in patients with schizophrenia. DISCLOSURE OF INTEREST: None Declared