During recent decades, much evidence has been accumulated concerning the neuroendocrine basis of schizophrenia. Recently, research has focused on stress hormones, with cortisol being the most widely researched, during the prodromal phase of psychosis. Thus, the present study aims to systematically review the evidence concerning the role of cortisol in patients at risk for psychosis mental state and its associations with psychopathological correlates. We systematically reviewed the published reports referring to both 'at clinical risk for psychosis' and 'at genetic risk for psychosis' mental state. Sixteen studies were identified. A trend towards increased cortisol levels in saliva emerged. Findings concerning cortisol levels in the blood were minimal and less consistent. The longitudinal studies, though with divergent results, hinted towards upregulation of cortisol secretion prior to psychotic conversion. Regarding cortisol's reactivity, evaluated through neuroendocrine, psychosocial and naturalistic stressors, the findings were minimal and divergent. The hypothesized relation of psychotic symptomatology with cortisol in subjects at risk for psychosis was not confirmed by the majority of the studies. On the contrary, the anxiety parameter and stress-intolerance index were both positively associated with cortisol. In conclusion, the published reports related to the evaluation of cortisol levels/ function at prodrome are hitherto minimal. Although the evidence favors cortisol's participation in the pathophysiology of psychosis, the exact cause-effect sequence and the intertwining of cortisol with psychopathology are still unclear.

Psoriasis constitutes one of the most representative examples of psychosomatic disorders. The published work investigating the psychological parameters and the way they interact during the course of the disease is extensive, whereas only a few studies have focused on the neuroendocrine framework of psoriasis. In the present study, the objective was to investigate the neuroendocrine parameters of psoriasis and the way they interact with psychopathological and immune variables. Patients with psoriasis (n=24) and the same number of matched healthy controls underwent psychiatric evaluation with interviews and psychometric questionnaires. Both of the groups underwent the corticotropin-releasing hormone (CRH) test and the dexamethasone suppression test (DST) to investigate functional parameters of the hypothalamus-pituitary-adrenal (HPA) axis. The evaluation of immune variables included the estimation of the distribution of T-cell and natural killer lymphocytes. Levels of depressive and anxiety features were increased within subjects with psoriasis and they were significantly correlated with stressful life events and the extent of the disease. The adrenocorticotrophic hormone and cortisol levels increased after CRH infusion without significant differences between the two groups and the psoriatic subjects' cortisol suppression after DST was within normal range, though relatively blunted. No significant correlations were identified among neuroendocrine, psychopathological and immune parameters. No particular neuroendocrine profile has been identified among psoriatic patients and the hypothesized interaction with psychopathological and immune parameters was not replicated. Nevertheless, it is still premature to exclude the possibility that a subtle latent alteration of the HPA axis function might exist, in psoriasis, either stemming from the psychopathology or from the disease per se.

The aim of the study was to determine circulating cytokines, cortisol and Insulin-like Growth Factor (IGF)-1, known for their involvement in inflammation, in male patients with First Episode Psychosis (FEP) and subjects at Ultra High Risk (UHR) for Psychosis. The FEP group presented increased pro-inflammatory cytokines (TNF-α, IFN-γ, ΤNF-β) as well as increased anti-inflammatory cytokine (IL-4) compared with Healthy Controls (HC). The UHR group showed increased IL-4 against HC. In contrast, none of the groups did show deviation from normality in either cortisol or IGF-1 levels. These preliminary findings support the cytokines' role in the inflammatory hypothesis in psychosis.