Blood viscosity and inflammation in first-episode and acute exacerbations of schizophrenia: A case-control study with healthy controls

Introduction: Elevated proinflammatory status and alterations in blood flow, both of which are associated with the pathophysiology of schizophrenia, may be linked with an increased risk of cardiovascular diseases. However, such a relationship at different acute stages of schizophrenia has not been evaluated. We aimed to examine whether blood viscosity and systemic inflammatory status varied between first-episode schizophrenia (FES) and acute exacerbations of schizophrenia. Methods: Fifty-two patients with FES, 69 schizophrenia patients with acute exacerbation (S-AE) and 56 healthy controls (HC) were included in the study. Whole blood viscosity (WBV) was calculated according to de Simone’s formula at low and high shear rates (LSR and HSR). Systemic immune-inflammation index (SII) and systemic inflammatory response index (SIRI) were calculated from hemogram screening data at admission. Results: When adjusted for age, WBV at both LSR and HSR were significantly decreased in both FES and S-AE groups compared to HCs. Systemic inflammatory response index was significantly higher in FES patients than in the S-AE and HC groups. Total cholesterol (TC) and WBV at HSR were correlated in patients. Total cholesterol predicted WBV at LSR in patients with FES whereas other independent variables including age and SIRI did not. Conclusion: Both first and subsequent episodes of schizophrenia are associated with reduced blood viscosity. Increased inflammatory status may not fully explain such a relationship. Extrapolation of hemorheological characteristics in schizophrenia may help to stratify cardiovascular risk and reflect the pathophysiological process in the early and later stages of schizophrenia

Blood viscosity and inflammatory indices in treatment-resistant schizophrenia: A retrospective cross-sectional study

Objective: Alterations in blood flow and inflammation may be associated with the treatment response of psychotic disorders. However, changes in blood viscosity in patients with treatment-resistant schizophrenia (TRS) have yet to be studied. We examined whether blood viscosity and systemic inflammatory status varied between patients with TRS, remitted schizophrenia, and healthy subjects.Method: Forty patients with TRS, 40 remitted schizophrenia patients, and 43 age- and gender-matched healthy controls were enrolled in this retrospective file review study. Whole blood viscosity (WBV) was calculated according to de Simone's formula at low and high shear rates (LSR and HSR, respectively). Complete blood count (CBC) markers of inflammation were recorded through screening data at admission.Results: In patients with TRS, WBV at both LSR and HSR was significantly decreased, whereas all CBC markers of inflammation were significantly increased compared to controls. Remitted patients had significantly decreased WBV at HSR than controls. There was no significant correlation between blood viscosity and CBC markers in patients. According to the regression models, the systemic immune-inflammation index (& beta;=0.578) and monocyte-to-lymphocyte ratio (& beta;=1.844) were significantly associated with WBV at LSR in multivariate analyses, whereas the Positive and Negative Syndrome Scale (PANSS) Positive subscale (& beta;=-0.330) was significantly associated with WBV at HSR in univariate analyses in the patient sample.Conclusion: TRS, associated with decreased blood viscosity and increased inflammatory status, may not fully explain such a reflect the pathophysiological process underlying treatment responsiveness as well as cardiovascular morbidity

Investigating the effects of glucose and lipid metabolism on neuronal structure using optical coherence tomography in treatment-resistant schizophrenia

Objective:The effects of metabolic changes on neural structures in the later stages of schizophrenia remain unknown. Alterations in glucose and lipid metabolism could impact disease progression. This study aims to investigate the effects of glucose and lipid metabolism on neuronal structures in treatment-resistant schizophrenia using optical coherence tomography (OCT), glycogenic proteins, and cholesterol values.Method:The study included 39 schizophrenia patients with remission, 43 treatment-resistant schizophrenia (TRS) patients, and 40 healthy controls (HC). Optical coherence tomography (OCT) was performed on all participants. Serum samples were collected to determine fasting glucose, Low-Density Lipoprotein (LDL), High-Density Lipoprotein (HDL), triglycerides, total cholesterol, fasting insulin, and Insulin-like Growth Factor 1 (IGF-1) levels. Results: IGF-1 levels in TRS patients were higher than those in the remission group. Additionally, the thickness of the inferior retinal nerve fiber layer (RNFL), superior RNFL, and global RNFL regions was significantly lower in the TRS group than in the HC group.Conclusion: While OCT measurements and elevated IGF-1 levels indicate neural thinning in treatment-resistant schizophrenia, there was no observed effect from lipid and glucose metabolism on this phenomenon

Can the imbalance between neurotrophic and apoptotic proteins be the "beware the ides of march" for unaffected relatives of schizophrenia patients?

Schizophrenia (SZ) is a mental disorder with a strong genetic basis as well as epigenetic aspects. Siblings of patients with SZ can share certain endophenotypes with the patients, suggesting that siblings may be important for distinguishing between trait and state markers. In the current study, we aimed to characterize the balance between pro-BDNF/mature BDNF and its receptors p75NTR/TrkB, which are tPA-BDNF pathways proteins and are thought to play a role in synaptic pruning, as a possible endophenotype of schizophrenia. Forty drug-naive patients with first-episode psychosis (FEP) matched for age, gender, and level of education, 40 unaffected siblings (UAS) of patients with FEP, and 67 healthy controls (HC) were included in the study. Blood samples were collected from all participants to determine BDNF, pro-BDNF, TrkB and p75NTR, PAI1, tPA, ACTH, and cortisol levels. We showed that levels of proteins of the tPA-BDNF pathway as well as the pro-BDNF/m-BDNF and p75NTR/TrkB ratios could successfully differentiate FEP and their siblings from the HCs by using ROC analysis. Plasma levels of m-BDNF were found to be the lowest in the healthy siblings and highest in the HCs with statistically significant differences between all 3 groups. The plasma level of pro-BDNF in the HC group was similar to the FEP patients, the same in the healthy siblings of the FEP patients. Our data support the hypothesis that imbalance between neurotrophic and apoptotic proteins might occur in SZ and this imbalance could be an endophenotype of the disease.University of (University of Health Sciences Turkey) Research Projects Uni