Serum PGE2, 15d-PGJ, PPARγ and CRP levels in patients with schizophrenia.

Many hypotheses have been proposed for the development of schizophrenia, including the one proposing that exogenous and endogenous factors are linked to inflammatory processes. There is strong evidence about the immunological and inflammatory dysfunction in schizophrenia. In this study, we aimed to measure serum 15-deoxy-delta(12,14)-prostaglandin J (15d-PGJ), peroxisome proliferator-activated receptor gamma(PPARγ), prostaglandin E2 (PGE2) and C-reactive protein (CRP) levels. Forty-four patients and 39 healthy volunteers were included in the study. Serum PGE2, 15d-PGJ, PPARγ and CRP levels were measured in both the groups. Demographic data forms were filled out for the patient group, and the Positive and Negative Syndrome Scale, Clinical Global Impression-Severity scale and Calgary Depression scale were used to assess patients' clinical status. Serum PGE2, 15d-PGJ and PPARγ levels were found to be significantly lower in patients with schizophrenia than in healthy controls. There was no significant relationship between the serum PGE2, 15d-PGJ and PPARγ levels and CRP levels.In this study, the evidence of systemic inflammatory conditions in patients with schizophrenia was found. The duration of the disease has been found to be the only variable that independently affects all three biomarker levels in the patients with schizophrenia.

Thiol/disulphide homeostasis in manic episode and remission phases of bipolar disorder.

PURPOSE: Bipolar disorder (BD) is a chronical psychiatric disorder of which pathophysiology was demonstrated to be related with oxidative stress. Thiol-disulphide homeostasis is an indicator of oxidative balance. This study aims to investigate thiol-disulphide homeostasis in BD. MATERIALS AND METHODS: 27 patients in manic episode (MA), 29 patients in remission (RE) and 60 healthy participants (HC) were included to the study. Serum native thiol and total thiol levels were measured with a novel colorimetric, automated method. The disulphide levels and disulphide/native thiol ratios were also calculated from these measured parameters. RESULTS: Native thiol levels and total thiol levels of both MA and RE groups were lower than HC. No significant difference detected between MA and RE in terms of native thiol levels and total thiol levels. Disulphide levels and disulphide/native thiol ratio was detected statistically similar between three groups. CONCLUSION: Our results support the oxidative imbalance theory in pathophysiology of BD. Further studies with larger sample sizes are needed for being able to understand these pathways in detail and use them as a target of treatment.

Thiol/disulphide homeostasis in schizophrenia patients with positive symptoms.

INTRODUCTION: This study aims to investigate the dynamic thiol/disulphincide homeostasis in patients with schizophrenia who have positive psychotic indications. MATERIALS AND METHODS: Forty-four patients (26 males, 18 females; mean age = 34.40 ± 8.98 years) accepted at the Department of Psychiatry of the Ankara Numune Training and Research Hospital and 33 healthy controls (15 males, 18 females; mean age of 30.30 ± 8.48 years) were included in the study. Serum native thiol and total thiol were measured with a novel colorimetric, automated method. The disulfide levels and disulfide/native thiol ratios were also calculated from these measured parameters. RESULTS: Serum native thiol and the total thiol concentration were significantly lower in schizophrenia compared with the control group (p < .05). Disulphide levels and disulfide/native thiol ratios were significantly higher in schizophrenia compared with the control group (p < .05). When the patients were divided into two groups according to those who used medication and those who did not for the last two months, it was found to be significantly higher in those who used disulfide and disulfide/native thiol medication than those who did not use medication. CONCLUSION: The disulfide/native thiol ratio in patients with schizophrenia who have been using medication for the last 2 months has been found to be significantly higher than controls who have not been using medication, may be indicating that the level of native thiol does not increase in a correlation as high as the increase in disulfide levels. It demonstrates that thiol/disulfide equilibrium has shifted towards the disulfide. The excess disulfide amounts might associated with both disease itself and the using medication.

The association of serum nesfatin-1 and ghrelin levels with metabolic syndrome in patients with schizophrenia.

Nesfatin-1 and ghrelin are two hormones which has opposite effects and play role in food intake. This study was planned on the idea that both metabolic syndrome and psychiatric disorders are associated with nesfatin-1 and ghrelin. In this study, it was aimed to investigate the levels of ghrelin and nesfatin-1 in patients with schizophrenia, by taking confounding factor as the metabolic syndrome (MS). 55 patients with schizophrenia and 33 healthy controls were included in the study.11 out of the 55 patients (%20) has MS. Serum ghrelin and nesfatin-1 levels of schizophrenia patients with MS have been compared with both healthy controls and schizophrenia patients without MS. Patients with schizophrenia had significantly higher serum nesfatin-1 levels compared to healthy controls. But serum ghrelin levels was not different in both groups. Serum nesfatin-1 concentrations were significantly higher in the schizophrenia patients with MS (10.51-350.8pg/ml) with respect to the healthy control group (4.86-68.91pg/ml). There was no significant statistical difference between the three groups in terms of ghrelin levels. Our findings suggests that, MS presence also contributed to significantly high levels of nesfatin-1 level. Nesfatin-1 may have a part in a novel studies regarding the treatment of schizophrenia and its metabolic effects.

Serum TNF-related weak inducer of apoptosis (TWEAK) and TNF-related apoptosis-inducing ligand (TRAIL) levels of patients with bipolar disorder in manic episode, in remission and healthy controls.

TNF-related weak inducer of apoptosis (TWEAK) and TNF-related apoptosis-inducing ligand (TRAIL) are members of TNF superfamily, which has various roles in immunologic and inflammatory reactions in the organism. Pathophysiology in bipolar disorder is still under investigation and altered serum levels of cytokines are often encountered. Aim of this study is to detect serum TWEAK and TRAIL levels of patients with bipolar disorder and healthy controls. For this purpose, 55 patients with bipolar disorder -27 manic episode (ME), 28 remission (RE) and 29 healthy controls (HC) were included. TWEAK levels of ME and RE groups were significantly lower than HC. TWEAK levels of bipolar patients (BP) were also lower than HC. TRAIL levels of ME, RE, HC groups and BP, HC groups were statistically similar. In our knowledge, this is the first study concerning about TWEAK and TRAIL levels in bipolar disorder and our results pointed that TWEAK-related immune response might be impaired in bipolar disorder, but our study fails to eradicate the confounders such as medication, smoking and body mass index. Studies having larger samples and limited confounders are needed to be able to evaluate these changes better and detect possible alterations about TRAIL and other TNF superfamily members.

Evaluation of Oxidative Stress in Bipolar Disorder in terms of Total Oxidant Status, Total Antioxidant Status, and Oxidative Stress Index.

INTRODUCTION: Bipolar disorder is one of the most debilitating psychiatric disorders characterized by disruptive episodes of mania/hypomania and depression. Considering the complex role of biological and environmental factors in the etiology of affective disorders, recent studies have focused on oxidative stress, which may damage nerve cell components and take part in pathophysiology. The aim of the present study was to contribute to the data about oxidative stress in bipolar disorder by detecting the total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels of manic episode (ME) and euthymic (EU) patients and by comparing these results with those of healthy controls (HCs). METHODS: The study population consisted of 28 EU outpatients meeting the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) criteria for bipolar disorder I and 23 inpatients who were currently hospitalized in a psychiatry ward with the diagnosis of the bipolar disorder ME according to the DSM-5 criteria. Forty-three healthy subjects were included in the study as the control group (HC). Serum TAS, TOS, and OSI levels of all the participants were determined. RESULTS: Statistical analysis of serum TAS, TOS, and OSI levels did not show any significant differences between the ME patients, EU patients, and HCs. Comparison between the bipolar disorder patients (ME+EU) and HC also did not reveal any statistically significant difference between these two groups in terms of serum TAS, TOS, and OSI levels. CONCLUSION: To date, studies on oxidative stress in bipolar disorder have led to controversial results. In the present study, no statistically significant difference was detected between the oxidative parameters of bipolar disorder patients and HCs. In order to comprehensively evaluate oxidative stress in bipolar disorder, further studies are needed.

TNF-related weak inducer of apoptosis (TWEAK) levels in schizophrenia.

Members of tumor necrosis factor (TNF) superfamily have roles in many biological events and pathogenesis of central nervous system (CNS) diseases. A relatively recently found member of this family, TNF-related weak inducer of apoptosis (TWEAK) have importance both in development of pathological CNS processes and as a target for the treatment of these diseases. The aim of this study was to investigate whether TWEAK's plasma levels are different in patients with schizophrenia. For this purpose plasma TWEAK levels of 44 patients diagnosed with schizophrenia and control group of 40 healthy individuals were compared. Although numerical difference was found between TWEAK levels of patients and controls it was not statistically significant. When we tested for female and male patients and controls seperately, TWEAK levels of male patients were significantly lower than male controls. As far as we know this is the first study that investigates levels of TWEAK in patients with schizophrenia. Although we did not find statistically significant results in our study, we believe that difference could be found in future studies with higher number of subjects. Researches with non-studied TNF superfamily members like TWEAK and TNF-related apoptosis-inducing ligand (TRAIL) could contribute to the understanding of immune-cytokine related hypotheses of schizophrenia.

An alternative marker of low-density lipoprotein cholesterol in coronary artery disease: non-high-density lipoprotein cholesterol.

BACKGROUND/AIM: Dyslipidemia is one of the most important risk factors for coronary artery disease (CAD), and low-densitylipoprotein cholesterol (LDL-C) is used to measure dyslipidemia. Non-high-density lipoprotein cholesterol (non-HDL-C) seems to be an alternative parameter to LDL-C as it is not influenced by triglyceride (TG) levels. The aim of this study is to compare non-HDL-C and LDL-C levels as risk markers in CAD patients. MATERIALS AND METHODS: One hundred and ten CAD patients and 42 individuals with normal coronary angiography results were included in this study. Patients were divided into 2 groups: TG < 200 mg/dL (n = 75) as group 1 and TG > 200 mg/dL (n = 35) as group 2. Total cholesterol (TC), TG, and HDL-C levels were analyzed with a Roche Modular P800 autoanalyzer. LDL-C and non-HDL-C levels were calculated. RESULTS: There were statistically significant differences in TC, TG, HDL-C, and non-HDL-C levels when the groups were compared. Non-HDL-C levels of group 2 were statistically higher than those of group 1 and the control group. There was no significant difference in LDL-C levels between the groups. CONCLUSION: Non-HDL-C levels are better risk markers than LDL-C levels, especially in patients with TG > 200 mg/dL, and non-HDL-C levels should be taken into consideration when evaluating the risk of CAD.

Correlation between total vitamin D levels and psychotic psychopathology in patients with schizophrenia: therapeutic implications for add-on vitamin D augmentation.

OBJECTIVES: Vitamin D deficiency is one of the implicated factors in ethio-pathogenesis of schizophrenia. Low serum vitamin D levels have been reported in many schizophrenia studies. However, the question is still not answered: Is there a correlation between disease activity and serum vitamin D levels? This is the first study evaluating the relationship between serum total vitamin D levels and disease activity, by comparing total vitamin D levels in two schizophrenia groups abruptly different in terms of disease activity. METHODS: 41 patients with schizophrenia in remission, 40 patients with schizophrenia those in an acute episode and 40 age- and sex -matched controls with no major psychopatology were recruited in this study. Positive and Negative Syndrome Scale (PANSS) and the Clinical Global Impression - Severety scale (CGI-S) were used to evaluate disease activity. A demographic data form that included entries on age, gender, ethnicity, weight, skin color, daily duration of sun exposure and nutritional assessment were used. Blood samples were taken from all patients and controls. Total vitamin D (D2+D3), calcium, phosphor, parathyroid hormone values were measured. RESULTS: Patients in an acute episode had significantly lower vitamin D levels compared to patients in remission and to healthy controls (in terms of median values respectively, 7.18, 15.03, 15.02, p < 0.001). We observed negative and moderate correlations between vitamin D levels and CGI scores (r = -0.624, p < 0.001), vitamin D levels and PANNS scores (r = -0.508, p < 0.001). There were no significant differences between groups in terms of serum P, Ca and PTH levels (p = 0.099, p = 0.943, p = 0.762). We could not detect any significant impact of weekly duration of sun exposure, skin color, ethnicity or nutrition on total vitamin D levels. CONCLUSIONS: Even though important factors for vitamin D synthesis were similar, there was severe vitamin D deficiency in patients presenting with an acute episode, significantly different from those in remission. Is vitamin D deficiency the result or the cause of an acute episode? Our results contribute to the idea that vitamin D deficiency and schizophrenia may have interactions with an unknown pathway. Present data points out a possible influence at a genomic level. Future trials may investigate this association with longer follow up. We recommend that, serum vitamin D levels should be measured in patients with schizophrenia especially in long term care. Appropriate further treatment with add-on vitamin D supplements and diets that are rich in vitamin D should be considered.