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Prieto M.L.,Mayo Clinic Depression Center | Prieto M.L.,University of Los Andes, Chile | Cuellar-Barboza A.B.,Mayo Clinic Depression Center | Cuellar-Barboza A.B.,Autonomous University of Nuevo Leon | And 9 more authors.
Acta Psychiatrica Scandinavica | Year: 2014

Objective: To review the evidence on and estimate the risk of myocardial infarction and stroke in bipolar disorder. Method: A systematic search using MEDLINE, EMBASE, PsycINFO, Web of Science, Scopus, Cochrane Database of Systematic Reviews, and bibliographies (1946 - May, 2013) was conducted. Case-control and cohort studies of bipolar disorder patients age 15 or older with myocardial infarction or stroke as outcomes were included. Two independent reviewers extracted data and assessed quality. Estimates of effect were summarized using random-effects meta-analysis. Results: Five cohort studies including 13 115 911 participants (27 092 bipolar) were included. Due to the use of registers, different statistical methods, and inconsistent adjustment for confounders, there was significant methodological heterogeneity among studies. The exploratory meta-analysis yielded no evidence for a significant increase in the risk of myocardial infarction: [relative risk (RR): 1.09, 95% CI 0.96-1.24, P = 0.20; I2 = 6%]. While there was evidence of significant study heterogeneity, the risk of stroke in bipolar disorder was significantly increased (RR 1.74, 95% CI 1.29-2.35; P = 0.0003; I2 = 83%). Conclusion: There may be a differential risk of myocardial infarction and stroke in patients with bipolar disorder. Confidence in these pooled estimates was limited by the small number of studies, significant heterogeneity and dissimilar methodological features. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Source


Sarrazin S.,University Paris - Sud | Etain B.,University Paris - Sud | Etain B.,French Institute of Health and Medical Research | Vederine F.-E.,University Paris - Sud | And 17 more authors.
Journal of Affective Disorders | Year: 2011

Background: Circadian rhythm instability and abnormalities of melatonin secretion are considered as trait markers of bipolar disorder. Melatonin is secreted by the pineal gland. We investigated pineal volume in patients with bipolar disorder, and expected to observe smaller than normal pineal glands in cases of bipolar disorder. Methods: The primary outcome was the total pineal volume measured for each pineal gland with T1 MRI sequence. Twenty patients with bipolar I and II disorder and twenty controls were recruited. Pineal glands with large cysts (type 3) were excluded. Results: After exclusion of individuals with type 3 cysts, 32 subjects were analyzed for total pineal volume (16 patients with bipolar disorder and 16 controls). Total pineal volume did not differ significantly between patients (total pineal volume = 115+/-54.3 mm 3) and controls (total pineal volume = 110+/-40.5 mm 3). Conclusions: Contrary to our hypothesis, no difference in total pineal volume between patients with bipolar disorder and healthy subjects was observed. These results indicate that the putative dysfunction of the pineal gland in bipolar disorder could be not directly related to an abnormal volume of the pineal gland. © 2011 Elsevier B.V. All rights reserved. Source


Geoffroy P.A.,French Institute of Health and Medical Research | Geoffroy P.A.,University of Lille Nord de France | Bellivier F.,FondaMental Foundation | Bellivier F.,University Paris Diderot | And 3 more authors.
Frontiers in Bioscience - Elite | Year: 2014

Bipolar disorder (BD) is a severe chronic multifactorial disease that requires maintenance therapy with mood stabilizers (MS). Even with medications, the rate of response among patients with BD is low and the risk of relapse is high. Therefore, in this context of the urgent need for reliable and reproducible predictors of individual responses to MS, pharmacogenetics research is expected to provide helpful progress. Most pharmacogenetic studies of MS have focused on the response to lithium with several good putative candidate genes but informative results are sparse. There have been few studies on valproate, lamotrigine or atypical antipsychotics. Overall, the results of pharmacogenomics studies have not provided sufficient data to change daily practices in BD significantly and further investigation is warranted to identify highly relevant genetic predictors of response their roles. Although progress still remains to be made, the clinical assessment of a subject including the identification of specific individual phenotypic and pharmacogenetic characteristics is likely to become a powerful instrument for the development of personalized therapies. Source


Hadley D.,Childrens Hospital of Philadelphia | Wu Z.-L.,Childrens Hospital of Philadelphia | Kao C.,Childrens Hospital of Philadelphia | Kini A.,Childrens Hospital of Philadelphia | And 134 more authors.
Nature Communications | Year: 2014

Although multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P 2.40E 09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P 3.83E 23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P 4.16 04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions. © 2014 Macmillan Publishers Limited. All rights reserved. Source


Lagerberg T.V.,University of Oslo | Icick R.,French Institute of Health and Medical Research | Icick R.,University Paris Diderot | Andreassen O.A.,University of Oslo | And 14 more authors.
Journal of Affective Disorders | Year: 2016

Objective Cannabis use disorders (CUD) may influence the course of bipolar disorder (BD), but key confounding factors such as tobacco smoking have not been adequately addressed. This study examined whether CUD was associated with a more severe illness course in tobacco smoking BD patients. Methods A sample of French and Norwegian tobacco smoking patients with BD I and II (N=642) was investigated. DSM-IV diagnoses and other characteristics were obtained through personal interviews using structured questionnaires. The association between CUD and illness course was assessed in regression analyses. Results In bivariate analyses, CUD was associated with earlier BD onset, higher frequency of manic (in BD I) and depressive episodes and hospitalizations per illness year, and a higher occurrence of psychotic episodes. After controlling for potential confounders, the relationships with earlier BD onset (B=-5.60 95% CI=-7.65 to -3.64), and increased rates of manic episodes (OR=1.93, 95% CI: 1.15 to 3.23) and hospitalizations (OR=2.93, 95% CI: 1.85 to 4.64) remained statistically significant. Limitations Despite the multivariate approach, differences between the two samples may lead to spurious findings related to hidden confounders. Substance use and mood episode information was collected retrospectively, and potential birth cohort effects could not be controlled for. Conclusion Studies have found associations between tobacco smoking and poorer outcomes in BD. In this study on tobacco smoking BD patients we report an association between CUD and illness severity, suggesting that CUD exacerbates the disease evolution independently of tobacco smoking. Specific treatment and prevention programs addressing CUD in BD patients are warranted. © 2015 Elsevier B.V. All rights reserved. Source

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