BackgroundAlthough clozapine is an effective option for treatment-resistant schizophrenia (TRS), there are still 1/3 to 1/2 of TRS patients who do not respond to clozapine. The main purposes of this randomized, double-blind, placebo-controlled trial was to explore the amisulpride augmentation efficacy on the psychopathological symptoms and cognitive function of CTRS patients. MethodsA total of 80 patients were recruited and randomly assigned to receive an initial clozapine plus amisulpride or clozapine plus placebo. Positive and Negative Syndrome Scale (PANSS), Scale for the Assessment of Negative Symptoms (SANS), Clinical Global Impression (CGI) scale scores, Repeatable Battery for the Assessment of Neuropsychological Status (RBANS), Treatment Emergent Symptom Scale (TESS), laboratory measurements and electrocardiograms (ECG) were performed at baseline, week 6, and week 12. ResultsCompared with clozapine plus placebo group, clozapine plus amisulpride had lower PANSS total score, positive subscore and general psychopathology subscore at week 6 and week 12 (all p Bonferroni< 0.01). Furthermore, compared with clozapine plus placebo group, clozapine plus amisulpride showed improved RBANS language score at week 12 (p Bonferroni< 0.001). Clozapine plus amisulpride group had a higher treatment response rate (p = 0.04), lower scores of CGI severity (CGI-S) and CGI efficacy (CGI-E) at week 6 and week 12 than clozapine plus placebo (all p Bonferroni< 0.05). There were no differences in BMI, QT intervals or laboratory measurements between the groups. Our results demonstrate that amisulpride augmentation therapy can safely improve the psychiatric symptoms and cognitive performance of CTRS patients. ConclusionsOur study indicates that amisulpride augmentation therapy has important clinical significance for the treatment of CTRS to improve clinical symptoms and cognitive function with tolerability and safety.Trial registrationClinicaltrials.gov identifier- NCT03652974. Registered 31 August 2018, https://clinicaltrials.gov/ct2/show/NCT03652974
BackgroundIncreasing evidence indicates that dysregulated TNF-α and oxidative stress (OxS) contribute to the pathophysiology of schizophrenia. Additionally, previous evidence has demonstrated sex differences in many aspects of schizophrenia including clinical characteristics, cytokines and OxS markers. However, to the best of our knowledge, there is no study investigating sex differences in the association between TNF-α, the OxS system, and their interaction with clinical symptoms in schizophrenia patients, especially in first-episode drug-naïve (FEDN) patients. MethodsA total of 119 FEDN schizophrenia patients and 135 healthy controls were recruited for this study. Serum TNF-α, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and malondialdehyde (MDA) were measured. The Positive and Negative Syndrome Scale (PANSS) was applied to evaluate psychotic symptoms. Two-way ANOVA, partial correlation analysis and multivariate regression analysis were performed. ResultsA sex difference in MDA levels was demonstrated only in healthy controls (F = 7.06, p Bonferroni = 0.045) and not seen in patients. Furthermore, only male patients had higher MDA levels than male controls (F = 8.19, p Bonferroni = 0.03). Additionally, sex differences were observed in the association of TNF-α and MDA levels with psychotic symptoms (all pBonferroni<0.05). The interaction of TNF-α and MDA was only associated with general psychopathology symptom in male patients (B = -0.07, p = 0.02). ConclusionOur results demonstrate the sex difference in the relationship between TNF-α, MDA, and their interaction with psychopathological symptoms of patients with schizophrenia.
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