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Frontiers in Psychiatry 2024There may be an interaction between viral hepatitis and psychiatric disorders during disease progression. Herein, we conducted Mendelian randomization (MR) to explore...
BACKGROUND
There may be an interaction between viral hepatitis and psychiatric disorders during disease progression. Herein, we conducted Mendelian randomization (MR) to explore the causal associations and mediators between viral hepatitis and psychiatric disorders.
METHODS
Genome-wide association studies summary data for viral hepatitis [including chronic hepatitis B (CHB) and chronic hepatitis C (CHC)] and psychiatric disorders (including depression, anxiety, schizophrenia, obsessive-compulsive disorder, bipolar disorder, and post-traumatic stress disorder) were obtained. Two-sample MR was performed to assess the causal associations between viral hepatitis and psychiatric disorders. Further, a mediation analysis was conducted to evaluate the potential mediators. Inverse-variance weighted, MR-Egger, and weighted median were used as the main methods, while a sensitivity analysis was performed to evaluate pleiotropy and heterogeneity.
RESULTS
There was no causal effect of CHB/CHC on psychiatric disorders, as well as psychiatric disorders on CHB. However, schizophrenia presented a causal effect on increased CHC risk [odds ratio (OR)=1.378, 95%CI: 1.012-1.876]. Further, a mediation analysis identified coffee consumption and body mass index as mediators in the effect of schizophrenia on CHC, mediating 3.75% (95%CI: 0.76%-7.04%) and 0.94% (95%CI: 0.00%-1.70%) proportion, respectively.
CONCLUSION
We revealed that schizophrenia patients faced a high risk of CHC, and insufficient coffee consumption and underweight could mediate the causal effect of schizophrenia on CHC. The prevention of hepatitis C might be a beneficial strategy for patients with schizophrenia. The right amount of nutrition supplements and coffee consumption might be part of a beneficial lifestyle in preventing the high CHC risk in patients with schizophrenia.
PubMed: 38881548
DOI: 10.3389/fpsyt.2024.1359080 -
Scientific Reports Jun 2024Smooth pursuit eye movements are considered a well-established and quantifiable biomarker of sensorimotor function in psychosis research. Identifying psychotic syndromes...
Smooth pursuit eye movements are considered a well-established and quantifiable biomarker of sensorimotor function in psychosis research. Identifying psychotic syndromes on an individual level based on neurobiological markers is limited by heterogeneity and requires comprehensive external validation to avoid overestimation of prediction models. Here, we studied quantifiable sensorimotor measures derived from smooth pursuit eye movements in a large sample of psychosis probands (N = 674) and healthy controls (N = 305) using multivariate pattern analysis. Balanced accuracies of 64% for the prediction of psychosis status are in line with recent results from other large heterogenous psychiatric samples. They are confirmed by external validation in independent large samples including probands with (1) psychosis (N = 727) versus healthy controls (N = 292), (2) psychotic (N = 49) and non-psychotic bipolar disorder (N = 36), and (3) non-psychotic affective disorders (N = 119) and psychosis (N = 51) yielding accuracies of 65%, 66% and 58%, respectively, albeit slightly different psychosis syndromes. Our findings make a significant contribution to the identification of biologically defined profiles of heterogeneous psychosis syndromes on an individual level underlining the impact of sensorimotor dysfunction in psychosis.
Topics: Humans; Male; Female; Pursuit, Smooth; Psychotic Disorders; Adult; Biomarkers; Young Adult; Bipolar Disorder; Middle Aged; Case-Control Studies; Adolescent
PubMed: 38879556
DOI: 10.1038/s41598-024-64487-6 -
Progress in Neuro-psychopharmacology &... Jun 2024The various pharmacological interventions, ranging from mood stabilizers and antipsychotics to antidepressants, reflect the diff/iculty of treating depressive/manic... (Review)
Review
BACKGROUND
The various pharmacological interventions, ranging from mood stabilizers and antipsychotics to antidepressants, reflect the diff/iculty of treating depressive/manic symptomatology of bipolar disorder (BD). Among a broad range of mechanisms implicated, immune dysregulation may contribute to the increased inflammation that influences the course of BD. Inflammatory, neurotrophic and oxidative stress factors may be identified as promising peripheral biomarkers in brain functioning, perhaps serving as predictors of an effective response to treatment for BD. The present systematic review aimed to examine the evidence supporting the pharmacotherapeutic value of inflammatory and neurotrophic biomarkers in BD.
METHODS
PubMed, PsychINFO, Scopus and Web of Science were searched from inception to May 2024 by two independent reviewers. A total of 40 studies with 3371 patients with diagnosis and intervention of BD were selected.
RESULTS
Inconsistencies in the effects of pharmacological treatments on the connection between the expected anti-inflammatory response and symptomatologic improvement were identified. Mood stabilizers (lithium), antipsychotics (quetiapine), antidepressants (ketamine) or their combination were described to increase both pro-inflammatory (TNFα, IL-6) and anti-inflammatory (IL-4, IL-8) factors. Other medications, such as memantine and dextromethorphan, autoimmune (infliximab) non-steroidal anti-inflammatory (aspirin, celecoxib) drugs, antidiabetics (pioglitazone), and even dietary supplementation (omega-3), or their combination, clearly decrease inflammatory factors (TNFα, IL-6, IL-1β, C-reactive protein) and/or increase the neurotrophic factor BDNF in BD patients.
CONCLUSION
Inflammation in BD requires further investigation to understand the underlying immunologic mechanism, to identify predictors of treatment response, and to make informed decisions about the use and development of more effective pharmacological interventions for BD.
PubMed: 38879067
DOI: 10.1016/j.pnpbp.2024.111056 -
International Journal of Bipolar... Jun 2024The recurrent mental illness bipolar disorder is a major burden on the healthcare system, which underlines the importance of research into this disease. Germany is one...
BACKGROUND
The recurrent mental illness bipolar disorder is a major burden on the healthcare system, which underlines the importance of research into this disease. Germany is one of the most productive countries in this research activity. This bibliometric analysis aims to outline the social and conceptual structure of the German research landscape on bipolar disorder over the last decade. Furthermore, we provide a short overview over current public funding.
RESULTS
Concerning the social structure, most of the German publications were collaboration projects, both with a national but also international orientation, in the latter case predominantly with countries of the global North. Analysis of the conceptual structure of German research activity identified psychiatric genetics, early recognition of bipolar disorder, neuroimaging, and pharmacological interventions as important topics within the field. In the context of a survey, only few publicly funded research projects were reported, many of which did not exclusively investigate bipolar disorder but followed a transdiagnostic approach.
CONCLUSIONS
Our bibliometric analysis revealed internationally well-networked German research activities on bipolar disorder. In stark contrast to its high prevalence and correspondingly high financial burden to the healthcare system, current grant support for research on this illness is strikingly low, particularly concerning the development of novel treatments.
PubMed: 38878206
DOI: 10.1186/s40345-024-00344-9 -
International Journal of Bipolar... Jun 2024Mitochondrial dysfunction is implicated in the neuropathology of bipolar disorder (BD). Higher circulating cell-free mitochondrial DNA (ccf-mtDNA), generally reflecting...
BACKGROUND
Mitochondrial dysfunction is implicated in the neuropathology of bipolar disorder (BD). Higher circulating cell-free mitochondrial DNA (ccf-mtDNA), generally reflecting poorer mitochondrial health, has been associated with greater symptoms severity in BD. The current study examines the association of serum ccf-mtDNA and brain structure in relation to youth BD. We hypothesized that higher ccf-mtDNA will be associated with measures of lower brain structure, particularly in the BD group.
METHODS
Participants included 40 youth (BD, n = 19; Control group [CG], n = 21; aged 13-20 years). Serum ccf-mtDNA levels were assayed. T1-weighted brain images were acquired using 3T-MRI. Region of interest (ROI) analyses examined prefrontal cortex (PFC) and whole brain gray matter, alongside exploratory vertex-wise analyses. Analyses examined ccf-mtDNA main-effects and ccf-mtDNA-by-diagnosis interaction effects controlling for age, sex, and intracranial volume.
RESULTS
There was no significant difference in ccf-mtDNA levels between BD and CG. In ROI analyses, higher ccf-mtDNA was associated with higher PFC surface area (SA) (β = 0.32 p < 0.001) and PFC volume (β = 0.32 p = 0.002) in the overall sample. In stratified analyses, higher ccf-mtDNA was associated with higher PFC SA within both subgroups (BD: β = 0.39 p = 0.02; CG: β = 0.24 p = 0.045). Higher ccf-mtDNA was associated with higher PFC volume within the BD group (β = 0.39 p = 0.046). In vertex-wise analyses, higher ccf-mtDNA was associated with higher SA and volume in frontal clusters within the overall sample and within the BD group. There were significant ccf-mtDNA-by-diagnosis interactions in three frontal and parietal clusters, whereby higher ccf-mtDNA was associated with higher neurostructural metrics in the BD group but lower neurostructural metrics in CG.
CONCLUSIONS
Contrasting our hypothesis, higher ccf-mtDNA was consistently associated with higher, rather than lower, regional neuralstructural metrics among youth with BD. While this finding may reflect a compensatory mechanism, future repeated-measures prospective studies evaluating the inter-relationship among ccf-mtDNA, mood, and brain structure across developmental epochs and illness stages are warranted.
PubMed: 38874862
DOI: 10.1186/s40345-024-00334-x -
Brain and Behavior Jun 2024Traumatic brain injury (TBI) refers to damage to brain tissue by mechanical or blunt force via trauma. TBI is often associated with impaired cognitive abilities, like... (Review)
Review
INTRODUCTION
Traumatic brain injury (TBI) refers to damage to brain tissue by mechanical or blunt force via trauma. TBI is often associated with impaired cognitive abilities, like difficulties in memory, learning, attention, and other higher brain functions, that typically remain for years after the injury. Lithium is an elementary light metal that is only utilized in salt form due to its high intrinsic reactivity. This current review discusses the molecular mechanisms and therapeutic and neuroprotective effects of lithium in TBI.
METHOD
The "Boolean logic" was used to search for articles on the subject matter in PubMed and PubMed Central, as well as Google Scholar.
RESULTS
Lithium's therapeutic action is extremely complex, involving multiple effects on gene secretion, neurotransmitter or receptor-mediated signaling, signal transduction processes, circadian modulation, as well as ion transport. Lithium is able to normalize multiple short- as well as long-term modifications in neuronal circuits that ultimately result in disparity in cortical excitation and inhibition activated by TBI. Also, lithium levels are more distinct in the hippocampus, thalamus, neo-cortex, olfactory bulb, amygdala as well as the gray matter of the cerebellum following treatment of TBI.
CONCLUSION
Lithium attenuates neuroinflammation and neuronal toxicity as well as protects the brain from edema, hippocampal neurodegeneration, loss of hemispheric tissues, and enhanced memory as well as spatial learning after TBI.
Topics: Brain Injuries, Traumatic; Humans; Neuroprotective Agents; Animals; Lithium; Brain; Lithium Compounds
PubMed: 38874089
DOI: 10.1002/brb3.3595 -
Cureus May 2024Affective disorders impose a significant burden on public health due to their high prevalence and associated suffering. This study addresses gaps in current literature...
INTRODUCTION
Affective disorders impose a significant burden on public health due to their high prevalence and associated suffering. This study addresses gaps in current literature and clinical practice by providing insights into medication usage trends, which can inform treatment strategies and optimize patient care. The study aims to investigate drug utilization patterns, particularly focusing on defined daily dose/1000/day, among individuals attending a psychiatric outpatient department of a tertiary care hospital.
METHODS
This cross-sectional, prospective drug utilization study included 600 affective disorder patients aged 18 years and above. The study period spanned 12 months, from March 2021 to February 2022. Data on demographics, diagnosis, treatment, and counseling were collected and analyzed using descriptive statistics.
RESULTS
Among the 600 patients analyzed, bipolar mood disorder was the most prevalent (239 patients, 39.83%), followed by depressive disorder (208 patients, 34.67%). Triple therapy was the most common prescription regimen, accounting for 308 encounters (51.33%). The average number of drugs per encounter was 3.75 ± 1.01. A combination of psychotherapy and medication counseling sessions was provided to 594 patients or their relatives, representing 99% of the total encounters.
CONCLUSION
The study highlights the prevalent use of triple therapy in managing affective disorders, especially bipolar mood disorder and mania disorder. Effective utilization of essential drug lists and comprehensive patient counseling underscores the importance of holistic care in psychiatric outpatient settings.
RECOMMENDATION
Given the high prevalence of triple therapy, further research into the efficacy and safety of this treatment approach is warranted. Additionally, continued emphasis on patient education and counseling can enhance treatment adherence and overall outcomes in individuals with affective disorders.
PubMed: 38872682
DOI: 10.7759/cureus.60290 -
Noro Psikiyatri Arsivi 2024Electroconvulsive therapy (ECT) is one of the biological therapies that is well tolerated and has a low risk of complications. Acute cardiovascular complications related...
INTRODUCTION
Electroconvulsive therapy (ECT) is one of the biological therapies that is well tolerated and has a low risk of complications. Acute cardiovascular complications related to ECT such as ventricular arrhythmia, myocardial infarction and cardiac arrest have been recorded. Increased frontal QRS-T (fQRS-T) angle was associated with ventricular arrhythmia, sudden cardiac death and total mortality. In this study, we aimed to evaluate the effect of ECT on the myocardium using electrocardiography (ECG) parameters such as fQRS-T angle, QRS duration, QT and QTc interval.
METHODS
A total of 108 patients diagnosed with bipolar disorder (n=36), depressive disorder (n=70) and schizophrenia (n=2) who underwent ECT were included in this study. 12-lead surface ECG of all patients were taken before the ECT, 15 min. after ECT and 24 hour after ECT.
RESULTS
QRS duration, QT interval and corrected QT (QTc) interval were not changed significantly during the follow-up period. However, we found that, fQRS-T angle was significantly increased 15 minutes after ECT compared to baseline angle (p<0.001). We also detected that this increase in fQRS-T angle 15 minutes after ECT was significantly reduced 24 hours after ECT (p=0.031). Meanwhile, there was no significant difference between baseline and 24th hour fQRS-T angle (p=0.154).
CONCLUSIONS
In our study, a significant increase in fQRS-T angle was observed 15 min after ECT. However, the fQRS-T angle was found to return to normal after 24 hours. Our findings may indicate that ECT does not have a permanent side effect on the risk of cardiovascular events according to the fQRS-T angle.
PubMed: 38868850
DOI: 10.29399/npa.28443 -
Noro Psikiyatri Arsivi 2024High mobility group box 1 protein (HMGB1) is a member of the molecular family known as damage-associated molecular patterns, which is implicated to have a role in...
INTRODUCTION
High mobility group box 1 protein (HMGB1) is a member of the molecular family known as damage-associated molecular patterns, which is implicated to have a role in neuroinflammation processes. In recent years, a growing number of studies have focused on the role of inflammation in Bipolar Disorder (BD). This study aimed to investigate the serum levels of HMGB1 and other inflammatory markers in patients with bipolar manic episodes compared to those in healthy controls (HC).
METHODS
A single-center, observational, case-control study was conducted. Thirty-five patients with BD in manic episodes and 35 HC were assessed. Young Mania Rating Scale (YMRS) was used to assess the symptom severity of the patient group. While inflammatory markers (such as HMGB1, C-reactive protein (CRP) and white blood cell count) were assessed at the first three and the last day of hospitalization in the patient group, they were evaluated once in HC. Levels of inflammatory markers were compared between (patient-HC) and within groups (before-after treatment).
RESULTS
No difference was observed in serum HMGB1 levels of bipolar patients with manic episodes compared to the HC (p>0.05). C-reactive protein levels of manic patients were higher than HC (p<0.001), and the difference persisted even after treatment (p=0.007). In addition, there was a significant positive correlation between CRP levels and antipsychotic drug dosage (r=0.382, p=0.024).
CONCLUSION
There were no differences in HMGB1 levels between bipolar patients with acute manic episode and HC. However, higher CRP levels in bipolar patients support the low-grade inflammation hypothesis in the etiology of BD.
PubMed: 38868848
DOI: 10.29399/npa.28599 -
PCN Reports : Psychiatry and Clinical... Dec 2023Jitteriness/anxiety syndrome is a recognized adverse effect observed during the initiation or change of dose in antidepressant treatment. Managing patients who develop...
BACKGROUND
Jitteriness/anxiety syndrome is a recognized adverse effect observed during the initiation or change of dose in antidepressant treatment. Managing patients who develop this syndrome remains a challenge. While escitalopram is a widely used antidepressant known to cause these symptoms, this report explores vortioxetine as a therapeutic alternative.
CASE PRESENTATION
Three distinct clinical scenarios were observed in patients who manifested jitteriness/anxiety syndrome while on escitalopram treatment for depression. Patient A was initiated on escitalopram and experienced an initial alleviation in depressive symptoms, but 3 months later displayed mood elevation, talkativeness, and increased activity, which disturbed his daily life. A transition to vortioxetine subsequently resolved the mood elevation. Patient B exhibited elevated mood, hyperactivity, irritability, and talkativeness just 6 days post-initiation of treatment with escitalopram. After the discontinuation of escitalopram and unsuccessful trials with aripiprazole, lurasidone, and lamotrigine, her depressive mood intensified, culminating in suicidal ideation. Starting vortioxetine led to a consistent improvement of her symptoms, and she resumed work and was emotionally stable. Patient C was initially diagnosed with bipolar disorder and faced a relapse into depression despite undergoing various treatments. After 2 weeks on escitalopram, she exhibited irritability and self-harm urges. Three months later, after being re-diagnosed with depressive disorders with anxious distress, vortioxetine was administered, which significantly reduced her depressive symptoms and allowed her to continue her education.
CONCLUSION
Vortioxetine presents as a promising therapeutic alternative that is worth considering for patients with escitalopram-induced jitteriness/anxiety syndrome.
PubMed: 38868737
DOI: 10.1002/pcn5.158