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Selected metabolites of kynurenine pathway and response to antipsychotic treatment in schizophrenia

Published online by Cambridge University Press:  23 March 2020

K. Szymona ,
H. Karakuła-Juchnowicz ,
M. Flis ,
T. Kocki ,
A. Urbanska ,
R. Kloc ,
Z. Szymona ,
W. Rosa  and
E.M. Urbańska
K. Szymona*
Affiliation:
Medical University of Lublin, Mental Health Outpatient Clinic- Children's University Hospital, Lublin, Poland
H. Karakuła-Juchnowicz
Affiliation:
Medical University of Lublin, Department of Clinical Neuropsychiatry Department of Psychiatry- Psychotherapy and Early Intervention, Lublin, Poland
M. Flis
Affiliation:
Medical University of Lublin, Department of Psychiatry- Psychotherapy and Early Intervention, Lublin, Poland
T. Kocki
Affiliation:
Medical University of Lublin, Laboratory of Cellular and Molecular Pharmacology- Department of Experimental and Clinical Pharmacology, Lublin, Poland
A. Urbanska
Affiliation:
Medical University of Lublin, Department of Psychiatry and Psychiatry Rehabilitation, Lublin, Poland
R. Kloc
Affiliation:
Medical University of Lublin, Laboratory of Cellular and Molecular Pharmacology- Department of Experimental and Clinical Pharmacology, Lublin, Poland
Z. Szymona
Affiliation:
PZ Cormay SA, Orphee Group, Lomianki, Poland
W. Rosa
Affiliation:
Lublin University of Technology, Faculty of Fundamentals of Technology- Department of Applied Mathematics, Lublin, Poland
E.M. Urbańska
Affiliation:
Medical University of Lublin, Laboratory of Cellular and Molecular Pharmacology- Department of Experimental and Clinical Pharmacology, Lublin, Poland
*
*Corresponding author.

Abstract

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Introduction

Deficit of glutamatergic transmission and aberrant function of kynurenine pathway, with disturbed synthesis of glutamate receptors antagonist, kynurenic acid (KYNA) and neurotoxic metabolite of kynurenine, 3-hydroxykynurenine (3-OH-KYN) have been implicated in the pathogenesis of schizophrenia.

Objectives

Demonstrated by others higher level of KYNA in the brain may cause relative deficiency of glutamate-mediate transmission with resulting behavioural and cognitive changes.

Aims

Search for predictors of satisfactory response to antipsychotic treatment based on the analysis of KYNA and 3-OH-KYN serum levels.

Methods

Fifty-three patients with chronic schizophrenia and 46 healthy individuals were enrolled in the study. Quantitative analyses of KYNA and 3-OH-KYN were performed using high-pressure liquid chromatography (HPLC) and electrochemical detection, respectively. Clinical assessments (PANSS, SANS, SAPS) and blood analyses were conducted at 3 time-points: during the active phase of disease, after 4 weeks of modified pharmacotherapy, and after reaching remission.

Results

In schizophrenia group, lower levels of KYNA (P = 0.002) and non-altered levels of 3-OH-KYN (p = 0.195), as compared to control, were detected during active phase of disease. Despite clinical improvement, no significant changes in the level of studied metabolites were observed later on. The initial level of 3-OH-KYN correlated negatively (r = –0.368; Spearman's rank) with clinical improvement (negative symptoms) (P < 0.05).

Conclusions

1. The peripheral dysregulation of kynurenine pathway metabolites in chronic schizophrenia manifests as relative increase in the ratio between neurotoxic 3-OH-KYN and neuroprotective KYNA. 2. The higher serum level of 3-OH-KYN during relapse of schizophrenia seems to predict poor response to antipsychotic treatment.

Disclosure of interest

The authors have not supplied their declaration of competing interest.

Type
EW559
Information
European Psychiatry , Volume 33 , Issue S1: Abstracts of the 24th European Congress of Psychiatry , March 2016 , pp. s264
Copyright
Copyright © European Psychiatric Association 2014
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