A Cardiovascular Risk Optimization Program in People With Schizophrenia: A Pilot Randomized Controlled Clinical Trial.

BACKGROUND: Cardiovascular disease is one of the leading causes of premature death in people with schizophrenia. Some modifiable factors that have been implicated include unhealthy lifestyle, medication side effects, and physical comorbidities. The goal of this study was to assess the efficacy of a 6-month, multifactorial cardiovascular risk intervention to reduce cardiovascular risk (CVR) in people with schizophrenia. METHODS: We conducted a 2-arm, parallel, randomized clinical trial in a regional mental health center. Participants with at least 1 poorly controlled cardiovascular risk factor (CVRF) (hypertension, diabetes mellitus, hypercholesterolemia, or tobacco smoking) were randomly assigned to the intervention group or to a control group. The subjects in the intervention group received a patient-centered approach that included promoting a healthy lifestyle, pharmacological management of CVRFs, psychotropic drug optimization, and motivational follow-up [Programa d'optimització del RISc CArdiovascular (PRISCA)]. The main outcome was change in CVR as assessed using the Framingham-REGICOR function, after 6 months compared with the baseline in both groups. RESULTS: Forty-six participants were randomly assigned to the PRISCA group (n=23) or the control group (n=23). The most prevalent CVRFs at baseline were hypercholesterolemia (84.8%) and tobacco smoking (39.1%). The PRISCA group showed a significant reduction in the REGICOR score (-0.96%; 95% CI: -1.60 to -0.32, P=0.011) after 6 months (relative risk reduction of 20.9%), with no significant changes in the control group (0.21%; 95% CI: -0.47 to 0.89, P=0.706). In the PRISCA group, low-density lipoprotein cholesterol also decreased significantly (-27.14 mg/dL; 95% CI: -46.28 to -8.00, P=0.008). CONCLUSION: A patient-centered, multifactorial cardiovascular risk intervention improved CVR in people with schizophrenia after 6 months, which was achieved mainly by improving the lipid profile.

Insight in Obsessive-Compulsive Disorder: Relationship With Sociodemographic and Clinical Characteristics.

Insight is considered a multidimensional concept and, in the context of obsessive-compulsive disorder (OCD), impairment in insight has been widely reported to be associated with severity and other clinical and sociodemographic variables. However, the studies concerning insight in OCD have produced heterogenous data as a result of the scales used to measure insight. To overcome this heterogeneity, the study presented here used 4 different widely used and validated insight scales. The objective was to evaluate various aspects of insight using these scales to identify the relationships between different aspects of insight and clinical and sociodemographic variables to assess which scale or scales might possess greater efficiency in clinical practice. For this purpose, a descriptive, observational, and cross-sectional study of 81 patients in treatment in a mental health center was conducted. Patients were evaluated using the Brown Assessment of Beliefs Scale, the Overvalued Ideas Scale, the Scale of Unawareness of Mental Disorders, the Yale-Brown Obsessive Compulsive Scale, the Clinical Global Impressions Scale, the Global Assessment of Functioning Scale, and the Rey-Osterrieth Complex Figure Test. The results reported significant relationships between insight and scores on the Yale-Brown Obsessive Compulsive Scale (Thoughts, Compulsions, and Total scales), Clinical Global Impressions Scale, and the Global Assessment of Functioning Scale, and significant differences with regard to sex, level of education, working status, and course of the disorder. A correlation analysis was conducted to assess the relationships among the 4 insight scales. The results of this analysis suggest that the scales that measure insight in a multidimensional way (Brown Assessment of Beliefs Scale and Overvalued Ideas Scale) provide more information about the severity of the disorder in patients with OCD.

Sociodemographic and Clinical Characteristics Associated with Suicidal Behaviour and Relationship with a Nurse-Led Suicide Prevention Programme.

Suicidal behaviour is a major public health problem that needs to be tackled by all health agents including mental health nurses. AIMS: The purpose of this study was to analyse the relationship between demographic and clinical characteristics and different kinds of suicidal behaviour with a nurse-led suicide prevention programme. METHODS: The design was a cross-sectional study, performed in the region of Osona (Catalonia) in the five-year period 2013-2017. Suicidal behaviour was classified as suicidal ideation, interrupted self-directed violence, suicide attempt or completed suicide. RESULTS: The sample included 753 patients (of whom 53 completed suicide) who experienced 931 suicidal behaviour episodes. Men represented only 38.4% of the sample but 81.1% of completed suicides. Mental disorders were associated with suicidal behaviour in 75.4% of the sample. Two thirds (66.4%) of the individuals (0.8% (n = 4) of whom completed suicide) were participants in a nurse-led suicidal behaviour case management programme. CONCLUSION: The main risk factors were being a woman for suicidal behaviour and being a man and being older for completed suicide. Mental disorders, widowhood and retirement were also associated with completed suicide. The completed suicide rate was lower among participants in the nurse-led programme.

Are the changes in the peripheral brain-derived neurotrophic factor levels due to platelet activation?

Brain-derived neurotrophic factor (BDNF) plays an important role in central nervous system development, neurogenesis and neuronal plasticity. BDNF is also expressed in several non-neuronal tissues, and it could play an important role in other processes, such as cancer, angiogenesis, etc. Platelets are the major source of peripheral BDNF. However, platelets also contain high amounts of serotonin; they express specific surface receptors during activation, and a multitude of pro-inflammatory and immunomodulatory bioactive compounds are secreted from the granules. Until recently, there was insufficient knowledge regarding the relationship between BDNF and platelets. Recent studies showed that BDNF is present in two distinct pools in platelets, in α-granules and in the cytoplasm, and only the BDNF in the granules is secreted following stimulation, representing 30% of the total BDNF in platelets. BDNF has an important role in the pathophysiology of depression. Low levels of serum BDNF have been described in patients with major depressive disorder, and BDNF levels increased with chronic antidepressant treatment. Interestingly, there is an association between depression and platelet function. This review analyzed studies that evaluated the relationship between BDNF and platelet activation and the effect of treatments on both parameters. Only a few studies consider this possible confounding factor, and it could be very important in diseases such as depression, which show changes in both parameters.

Prothrombotic platelet phenotype in major depression: downregulation by antidepressant treatment.

BACKGROUND: Serotonergic mechanisms have been suggested as a link between major depression and cardiovascular risk. We investigated the existence of a prothrombotic condition in depressed patients and its possible modulation during treatment with a selective serotonin-reuptake inhibitor (SSRI). METHODS: Modifications in a series of biomarkers of platelet and coagulation activation were evaluated in blood from 19 patients with a major depression disorder (MDD) at the time of diagnosis, and at 8 and 24 weeks of treatment with escitalopram. Response of blood aliquots recirculated through a thrombogenic surface was assessed in a thrombosis model. Results were compared with those of 20 healthy-matched controls. RESULTS: In comparison with controls, platelets from MDD patients showed elevated volumes (p<0.01), significantly enhanced aggregating response to arachidonic acid and augmented expression of GPIb, fibrinogen, factor V, and anionic phospholipids by flow cytometry (p<0.05). Clot firmness and procoagulant activity of platelet-associated tissue factor were also significantly elevated (p<0.05). Studies with circulating blood revealed increased fibrin formation in early diagnosed patients (71.1±9.5% vs. 45.8±5.3%; p<0.05 vs. controls). After 24 weeks of treatment with escitalopram, the majority of the alterations observed were normalized, except for a residual increased expression of GPIIbIIIa (p<0.05) and persistent alterations in thromboelatometic parameters. LIMITATIONS: Despite the reduced number of followed-up patients our findings were consistent reaching statistical significance. CONCLUSIONS: Our results reveal a prothrombotic phenotype in MDD patients. While continuous treatment with an SSRI downregulated the majority of the biomarkers analyzed, alterations in viscoelastic parameters of clot formation remained unaffected by the antidepressant treatment.

Changes in plasma and platelet BDNF levels induced by S-citalopram in major depression.

BACKGROUND: Neuroplastic processes are thought to be involved in the pathophysiology of major depression. It has been reported that serum brain-derived neurotrophic factor (BDNF) is decreased in depressed patients. OBJECTIVES: Compare BDNF levels in depressed patients and healthy controls in platelet poor plasma and in washed platelets. Observe the effects of 8- and 24-week treatment with S-citalopram on these levels. METHODS: We assessed the levels of BDNF in platelet poor plasma and in washed platelets from 18 major depression patients, and compared them with 14 healthy controls. Blood samples were obtained from patients before and during treatment (8 and 24 weeks) with a selective serotonin reuptake inhibitor, S-citalopram. RESULTS: A significant decrease in severity of depressive symptoms was observed from the first month of treatment with S-citalopram, and symptoms continued decreasing until the 6th month. Plasma BDNF levels in untreated patients appeared significantly increased (p<0.01) but reached values similar to those of controls at the 24th week. In contrast, levels of platelet BDNF appeared significantly decreased (p<0.05), but treatment also normalized levels so that values obtained were equivalent to those of controls. CONCLUSIONS: Untreated depressed patients showed increased plasma BDNF levels and decreased platelet BDNF levels, as compared with control subjects, and tend to normalize during treatment with S-citalopram for 24 weeks, with BDNF reaching levels similar to those in healthy controls at the 24th week in both samples. We observed that improvement in depressive symptoms was accompanied by normalization of plasma and platelet BDNF levels.