Abstract
Uric acid (UA) has been shown to have neuroprotective or neurotoxic properties, in relation to specific tissues and diseases that have been studied. Previous studies provided contradictory results on the role of UA in schizophrenia as a neurodegenerative disorder. The aim of this brief report was an additional analysis of UA sera levels in different phases of schizophrenia. Here, 86 patients with first-episode psychosis (FEP) vs. 45 patients with schizophrenia in relapse (SC in relapse) vs. 35 healthy control subjects (HC) were studied before and 1 month after antipsychotic therapy. Further, we aimed to explore the possible correlation of UA with scores presenting clinical features and with serum concentrations of the proinflammatory cytokines interleukin (IL)-6 and IL-17. When comparing the data between all three groups, we did not find significant differences in UA levels, either before or after the applied therapy. Also, comparing sera concentrations of UA in every single group, the analysis did not reveal statistically significant differences between FEP patients, but statistically, a significant difference was found in SC in relapse before and after treatment (334.71 ± 116.84 vs. 289.37 ± 109.15 μmol/L, p = 0.05). Uric acid serum levels correlated with negative sub-score (p = 0.001, r = 0.306), general sub-score (p = 0.015, r = 0.236), and total PANSS score (p = 0.009, r = 0.3) after 1 month of therapy. We have established a statistically significant positive correlation between serum concentrations of UA and IL-6 in exacerbation (p = 0.01, r = 0.220) and with IL-17 after treatment and in the stabilization of psychosis (p = 0.01, r = 0.34), suggesting potential cascades in different phases of schizophrenia that potentiate inflammation.
Highlights
Uric acid (UA) is the final oxidation product of the adenine- and guanine-based purine catabolic pathway and is considered as a risk factor of numerous pathological conditions [1]
This study aimed to examine whether serum levels of UA are altered in drug naïve patients with first-episode psychosis (FEP) and in patients with schizophrenia in relapse (SC in relapse) and compared them with levels measured in healthy control subjects (HC) subjects
When comparing serum UA levels in each group, the analysis did not reveal statistically significant differences between FEP patients (339.04 ± 175.97 vs. 304.01 ± 113.06 μmol/L, p = 0.207), but statistically, a significant difference was found in SC in relapse, before and after treatment (334.71 ± 116.84 vs. 289.37 ± 109.15 μmol/L, p = 0.05)
Summary
Uric acid (UA) is the final oxidation product of the adenine- and guanine-based purine catabolic pathway and is considered as a risk factor of numerous pathological conditions [1]. In a recent review paper, Morris and Maes [7] detailed that the immune-inflammatory response is associated with increased nitro-oxidative stress through the activation and involvement of macrophages, dendritic cells, neutrophils, T cells, B cells, and natural killer cells, is associated with increased nitro-oxidative stress. These redox-associated mechanisms modulated the production of provs. Uric acid is thought to have strong proinflammatory activity by triggering interleukin (IL)-1β-mediated inflammation via activation of the nucleotide oligomerization domain-like receptor protein (NLRP) 3 inflammasome, a multimolecular complex that plays a central role in many pathological inflammatory conditions [9, 10]. We have observed that the predomination of type 17 immune response facilitates the progression of inflammation and could be involved in the regulation of cognition [13]
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