Sexual dysfunction, as a noticeable adverse effect of atypical antipsychotic drugs (APDs) for the treatment of schizophrenia, has not been investigated in detail. A study was undertaken to investigate whether 28-day long treatment with clozapine, ziprasidone or sertindole (using a recommended daily dose for atypical antipsychotic therapy), induced histopathological changes both in rat testicles and prostate, changed the activity of the antioxidant defence system and altered blood testosterone and prolactin. Clozapine, ziprasidone and sertindole induced histopathological changes in rat testicular tissue, which could be attributed to a disturbed testicular antioxidant defence system in addition to an altered prolactin to testosterone ratio. None of the APD treatments induced histopathological changes in prostate. Our results demonstrate that APDs have the capacity to change both redox and endocrinological balance. One or both outcomes could underline testicular degeneration and disturbed spermatogenesis.

Chronic use of atypical antipsychotics may produce hepatic damage. Atypical antipsychotics, including clozapine, sertindole, and ziprasidone, are extensively metabolized by the liver and this process generates toxic-free radical metabolic intermediates which may contribute to liver damage. The aim of this study was to investigate whether clozapine, sertindole, or ziprasidone affected hepatic antioxidant defense enzymes which consequently led to disturbed redox homeostasis. The expression and activity of antioxidant enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), and glutathione-S-transferases (GST) were measured in rat livers at doses corresponding to human antipsychotic therapy. Clozapine increased activity of SOD types 1 and 2, GR and GST, but reduced CAT activity. Sertindole elevated activities of both SODs. In ziprasidone-treated rats only decreased CAT activity was found. All three antipsychotics produced mild-to-moderate hepatic histopathological changes categorized as regenerative alterations. No apparent signs of immune cell infiltration, microvesicular or macrovesicular fatty change, or hepatocytes in mitosis were observed. In conclusion, a 4-week long daily treatment with clozapine, sertindole, or ziprasidone altered hepatic antioxidant enzyme activities and induced histopathological changes in liver. The most severe alterations were noted in clozapine-treated rats. Data indicate that redox disturbances may contribute to liver dysfunction after long-term atypical antipsychotic drug treatment.

Even though inflammation theory has been introduced in the pathophysiology of psychosis almost a century ago, many of its aspects have remained unelucidated. Numerous studies have shown cytokine dysregulation in schizophrenia and a predominance of pro-inflammatory cytokines, but on another side, various cytokines in a pro-inflammatory group have different trends in all subtypes of schizophrenia. Alterations are also present in anti-inflammatory and regulatory cytokines, but findings are still not consistent. On the other hand, it is well known that abuse and neglect in childhood may be predictors of psychotic disorders, and childhood adversity is also associated with alterations of the immune and inflammatory response (through various mechanisms including HPA dysregulation as well). This review aims to analyze conducted studies and elucidate the link between childhood abuse, schizophrenia, and cytokine alterations. Putting together this complex psycho-immunological puzzle for the subgroup of schizophrenia-diagnosed patients with distinct immunological abnormalities and a history of childhood abuse can help us to answer the question about the future treatment of these patients.

Bipolar disorder (BD) and schizophrenia (SCH) are results of the complex interactions between genetic and environmental factors, and the underlying pathophysiology is not yet completely understood. The current diagnostic criteria for psychiatric diagnosis are based purely on clinical phenomenology and they are limited to psychiatrist judgment after a standardized clinical interview, with no precise biomarkers used to discriminate between the disorders. Besides gaps in the understanding and diagnosis of these diseases, there is also a need for personalized and precise approaches to patients through customized medical treatment and reliable monitoring of treatment response. To fulfill existing gaps, the establishment of disorder biomarker sets is a necessary step. LC-MS lipidomic blood sample analysis is one of the ongoing omics approaches. In the last ten years, several studies have identified alterations in lipid metabolism associated with BD and SCH, and this review summarizes current knowledge on their lipidomic patterns, which is essential for identifying lipid biomarkers. Currently, findings indicate decreases in plasmalogens and acyl-carnitines, along with increases in certain triacylglycerol species, shared by both conditions. In contrast, serum LC-MS lipidomic profiles of sphingolipids including ceramides could be unique to BD, indicating the need for further investigation in future studies.

Objective: Trazodone is an effective antidepressant. The present study was designed as a non-interventional open-label, multi-centre, post-marketing study. The aim of the study was to evaluate the therapeutic effectiveness and tolerability of trazodone retard formulation (Trittico^® retard) in everyday clinical practice. Methods: Two hundred and forty-two patients with depressive disorder from 19 different centres were included in the study. The antidepressant and anxyolitic effects were assessed using Hamilton anxiety rating scale 14 items version, Hamilton depression rating scale 14 items version and Clinical Global Impression Severity scale. Results: After only two weeks of therapy, a statistically significant improvement in the HAM-D score, was observed. This observation was maintained over the whole study period, up to the day 56. Conclusions: Our study points toward clinical effectiveness of the prolonged-release formulation of trazodone in the treatment of unselected depressed patients in real-world practice.

The introduction of a new psychopharmaceutical medication instead of the previous one always poses a certain challenge. In the case of antipsychotics (AP), these problems are considerably more complicated and are mainly caused by the question of dose equivalents, but also by the pharmacokinetic properties of the drug. In the case of partial dopamine D2 agonists, an additional issue is the possibility of deterioration when switching from the previous D2 antagonists to these drugs. Cross-titration is therefore generally recommended. Finally, due to the capsule form, it is not possible to increase the dose of cariprazine by less than 1.5 mg during titration. In this paper, we have presented our proposal to replace the most commonly used second-generation APs with the third-generation AP cariprazine. We have taken into account the dose equivalents, the pharmacological forms of the drugs and their pharmacokinetic and pharmacodynamic properties.