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Risk of myocardial infarction and stroke in bipolar disorder: a systematic review and exploratory meta-analysis.

https://arctichealth.org/en/permalink/ahliterature264104
Source
Acta Psychiatr Scand. 2014 Nov;130(5):342-53
Publication Type
Article
Date
Nov-2014
Author
M L Prieto
A B Cuéllar-Barboza
W V Bobo
V L Roger
F. Bellivier
M. Leboyer
C P West
M A Frye
Source
Acta Psychiatr Scand. 2014 Nov;130(5):342-53
Date
Nov-2014
Language
English
Publication Type
Article
Keywords
Bipolar Disorder - epidemiology
Denmark - epidemiology
Humans
Myocardial Infarction - epidemiology
Risk
Risk Assessment - methods - statistics & numerical data
Stroke - epidemiology
Sweden - epidemiology
Taiwan - epidemiology
United States - epidemiology
Abstract
To review the evidence on and estimate the risk of myocardial infarction and stroke in bipolar disorder.
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.
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; I(2)  = 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; I(2)  = 83%).
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.
PubMed ID
24850482 View in PubMed
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Y chromosome haplogroups in autistic subjects.

https://arctichealth.org/en/permalink/ahliterature31733
Source
Mol Psychiatry. 2002;7(2):217-9
Publication Type
Article
Date
2002
Author
S. Jamain
H. Quach
L. Quintana-Murci
C. Betancur
A. Philippe
C. Gillberg
E. Sponheim
O H Skjeldal
M. Fellous
M. Leboyer
T. Bourgeron
Author Affiliation
Laboratoire d'Immunogénétique Humaine, INSERM E021, Institut Pasteur, 75015 Paris, France.
Source
Mol Psychiatry. 2002;7(2):217-9
Date
2002
Language
English
Publication Type
Article
Keywords
Autistic Disorder - genetics
Child
Female
Genetic markers
Haplotypes
Humans
Male
Research Support, Non-U.S. Gov't
Sex Factors
Y Chromosome
Abstract
The male to female ratio in autism is 4:1 in the global autistic population, but increases to 23:1 in autistic subjects without physical or brain abnormalities.(1) Despite this well-recognised gender difference, male predisposition to autistic disorder remains unexplained and the role of sex chromosomes is still debated. Numerical and structural abnormalities of the sex chromosomes are among the most frequently reported chromosomal disorders associated with autism. However, genome scans have failed to detect linkage on the X chromosome(2,3,4) and this approach cannot study the non-recombining region of the Y chromosome. In this study, we searched for a specific Y chromosome effect in autistic subjects. Using informative Y-polymorphic markers, the Y chromosome haplotypes of 111 autistic subjects from France, Sweden and Norway were defined and compared with relevant control populations. No significant difference in Y-haplotype distribution between the affected and control groups was observed. Although this study cannot exclude the presence of a Y susceptibility gene, our results are not suggestive of a Y chromosome effect in autism.
PubMed ID
11840316 View in PubMed
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Additive effects of childhood abuse and cannabis abuse on clinical expressions of bipolar disorders.

https://arctichealth.org/en/permalink/ahliterature261461
Source
Psychol Med. 2014 Jun;44(8):1653-62
Publication Type
Article
Date
Jun-2014
Author
M. Aas
B. Etain
F. Bellivier
C. Henry
T. Lagerberg
A. Ringen
I. Agartz
S. Gard
J-P Kahn
M. Leboyer
O A Andreassen
I. Melle
Source
Psychol Med. 2014 Jun;44(8):1653-62
Date
Jun-2014
Language
English
Publication Type
Article
Keywords
Adult
Age of Onset
Alcoholism - epidemiology
Bipolar Disorder - epidemiology - physiopathology
Child
Child Abuse - statistics & numerical data
Female
France - epidemiology
Humans
Male
Marijuana Abuse - epidemiology
Middle Aged
Norway - epidemiology
Suicide, Attempted - statistics & numerical data
Abstract
Previous studies of bipolar disorders indicate that childhood abuse and substance abuse are associated with the disorder. Whether both influence the clinical picture, or if one is mediating the association of the other, has not previously been investigated.
A total of 587 patients with bipolar disorders were recruited from Norway and France. A history of childhood abuse was obtained using the Childhood Trauma Questionnaire. Diagnosis and clinical variables, including substance abuse, were based on structured clinical interviews (Structured Clinical Interview for DSM-IV Axis I disorders or French version of the Diagnostic Interview for Genetic Studies).
Cannabis abuse was significantly associated with childhood abuse, specifically emotional and sexual abuse (? 2 = 8.63, p = 0.003 and ? 2 = 7.55, p = 0.006, respectively). Cannabis abuse was significantly associated with earlier onset of the illness (z = -4.17, p
PubMed ID
24028906 View in PubMed
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Affective lability mediates the association between childhood trauma and suicide attempts, mixed episodes and co-morbid anxiety disorders in bipolar disorders.

https://arctichealth.org/en/permalink/ahliterature287299
Source
Psychol Med. 2017 Apr;47(5):902-912
Publication Type
Article
Date
Apr-2017
Author
M. Aas
C. Henry
F. Bellivier
M. Lajnef
S. Gard
J-P Kahn
T V Lagerberg
S R Aminoff
T. Bjella
M. Leboyer
O A Andreassen
I. Melle
B. Etain
Source
Psychol Med. 2017 Apr;47(5):902-912
Date
Apr-2017
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Adult Survivors of Child Adverse Events - psychology - statistics & numerical data
Age of Onset
Aged
Anxiety Disorders - epidemiology - physiopathology
Bipolar Disorder - epidemiology - physiopathology
Comorbidity
Female
France - epidemiology
Humans
Male
Middle Aged
Norway - epidemiology
Psychotic Disorders - epidemiology - physiopathology
Suicide, Attempted - psychology - statistics & numerical data
Young Adult
Abstract
Many studies have shown associations between a history of childhood trauma and more severe or complex clinical features of bipolar disorders (BD), including suicide attempts and earlier illness onset. However, the psychopathological mechanisms underlying these associations are still unknown. Here, we investigated whether affective lability mediates the relationship between childhood trauma and the severe clinical features of BD.
A total of 342 participants with BD were recruited from France and Norway. Diagnosis and clinical characteristics were assessed using the Diagnostic Interview for Genetic Studies (DIGS) or the Structured Clinical Interview for DSM-IV Axis I disorders (SCID-I). Affective lability was measured using the short form of the Affective Lability Scale (ALS-SF). A history of childhood trauma was assessed using the Childhood Trauma Questionnaire (CTQ). Mediation analyses were performed using the SPSS process macro.
Using the mediation model and covariation for the lifetime number of major mood episodes, affective lability was found to statistically mediate the relationship between childhood trauma experiences and several clinical variables, including suicide attempts, mixed episodes and anxiety disorders. No significant mediation effects were found for rapid cycling or age at onset.
Our data suggest that affective lability may represent a psychological dimension that mediates the association between childhood traumatic experiences and the risk of a more severe or complex clinical expression of BD.
PubMed ID
27894372 View in PubMed
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Genome-wide scan for autism susceptibility genes. Paris Autism Research International Sibpair Study.

https://arctichealth.org/en/permalink/ahliterature33398
Source
Hum Mol Genet. 1999 May;8(5):805-12
Publication Type
Article
Date
May-1999
Author
A. Philippe
M. Martinez
M. Guilloud-Bataille
C. Gillberg
M. Råstam
E. Sponheim
M. Coleman
M. Zappella
H. Aschauer
L. Van Maldergem
C. Penet
J. Feingold
A. Brice
M. Leboyer
L. van Malldergerme
Author Affiliation
INSERM U155, Université Paris VII, France.
Source
Hum Mol Genet. 1999 May;8(5):805-12
Date
May-1999
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Autistic Disorder - genetics
Child
Child, Preschool
Chromosomes, Human
Female
Genetic markers
Genetic Predisposition to Disease
Humans
Linkage (Genetics)
Male
Pedigree
Research Support, Non-U.S. Gov't
Abstract
Family and twin studies have suggested a genetic component in autism. We performed a genome-wide screen with 264 microsatellites markers in 51 multiplex families, using non-parametric linkage methods. Families were recruited by a collaborative group including clinicians from Sweden, France, Norway, the USA, Italy, Austria and Belgium. Using two-point and multipoint affected sib-pair analyses, 11 regions gave nominal P -values of 0.05 or lower. Four of these regions overlapped with regions on chromosomes 2q, 7q, 16p and 19p identified by the first genome-wide scan of autism performed by the International Molecular Genetic Study of Autism Consortium. Another of our potential susceptibility regions overlapped with the 15q11-q13 region identified in previous candidate gene studies. Our study revealed six additional regions on chromosomes 4q, 5p, 6q, 10q, 18q and Xp. We found that the most significant multipoint linkage was close to marker D6S283 (maximum lod score = 2.23, P = 0.0013).
Notes
Erratum In: Hum Mol Genet 1999 Jul;8(7):1353van Malldergerme L [corrected to Van Maldergem L]
PubMed ID
10196369 View in PubMed
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