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S596
25th European Congress of Psychiatry / European Psychiatry 41S (2017) S583–S644
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.918EV0589
Genetic determinants of psychic
resilience after a diagnosis of cancer
M. Christensen
1 , A.Drago
2 ,∗
1
Via University College, Via University College, Holstebro, Denmark
2
Psykiatrisk Forskningsenhed Vest, Department of Clinical Medicine,
Aarhus University, Herning, Denmark
∗
Corresponding author.
Introduction
Co-morbidity between cancer and psychiatric dis-
orders including adjustment disorder, depressive disorders or angst
can seriously influence the prognosis and the quality of life of
patients.
Aim
The identification of the psychological and biological profile
of patients at risk for such co-morbidity is not yet available. Classical
candidate genes such as the BDNF, the 5-HTLPR and genes whose
products are involved in inflammatory events have received some
attention, but results are inconclusive.
Object and methods
In the present review the association
between cancer and psychiatric disorders is reviewed, a focus on
the investigation of the Gene X environment and the epigenetic
control over the activation of the HPA axis is proposed as a tool to
refine the definition of the biologic profile at risk for co-morbidity
between psychiatry and cancer.
Results and conclusion
Anumber of genes and socio-demographic
variables that may influence risk to suffer from a psychiatric dis-
order after a diagnosis of cancer is identified and discussed. The
identification of such biologic and socio-demographic profile is
instrumental in the identification of subjects at risk of a double
diagnosis, both somatic and psychiatric. An early identification of
such profile riskwould pave theway to the implementation of early
intervention strategies.
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.919EV0590
Is 22q11.2 deletion syndrome a
genetic subtype of schizophrenia?
R. Hernandez Anton
1 ,∗
, H. De La Red Gallego
1, M. Gomez Garcia
1,
A. Alonso Sanchez
1, E. Mayor Toranzo
1, J.A. Blanco Garrote
1,
M. De Lorenzo Calzon
1, M. Hernandez Garcia
1, E. Dominguez
2,
F. Uribe Ladron De Cegama
1, V. Molina Rodriguez
11
Hospital Clinico Universitario Valladolid, Psiquiatria, Valladolid,
Spain
2
Hospital La Mancha Centro, Psiquiatria, Alcazar De San Juan, Spain
∗
Corresponding author.
Introduction
22q11.2 deletion syndrome is a primary immuno-
deficiency due to micro-deletion on the large arm of chromosome
22. Patients suffer from several anomalies, including metal illness,
that such the case we present, mean a warning sign for further
study.
Methods
Twenty-one years-old male, with psychotic symptoms,
typical of schizophrenia, behavioral disorders and mental con-
fusion, plus epileptic episodes and psychomotor agitation. Two
previous incomes with the diagnosis of psychotic disorder not oth-
erwise specified. Treated with anti-psychotics at low doses with
inter-episode stability.
Background
Prematurity, low birth weight, neonatal asphyxia,
generalized seizures, otitis and recurrent urinary tract infections,
hypernasal voice, poor academic performance, difficulty relating.
Physical examination: hypernasal voice, furred tongue, dysmorphic
faces, scoliosis, hipotanía, stereotypes, delusions, auditory halluci-
nationsd negative symptoms.
Results
We considered the possibility of a neurodevelopmental
disorder, with a multidisciplinary approach, resulting in the diag-
nosis of paranoid schizophrenia and velocardiofacial syndrome,
which had gone unnoticed. Mean doses of clozapine, haloperidol
and topiramate were used. He accepted psychiatry and other spe-
cialties follow-up, since it requires a complex andmultidisciplinary
approach.
Conclusions
Definition of velocardiofacial Syndrome and lack of
consensus on terminology:
– syndrome 22q11.2 DS as genetic subtype of schizophrenia?
Opportunity to study the pathogenesis of schizophrenia;
– the importance of a comprehensive approach to early diagnosis,
clinical improvement and preventing complications.
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.920EV0591
The genetic study of computer game
addiction
D. Mavani
1 ,∗
, V. Soldatkin
2, E. Mashkina
3, A. Dyachenko
1,
E. Karpova
1, O. Bukhanovskaya
11
Scientific Center for Treatment and Rehabilitation “Phoenix”,
Psychiatry department, Rostov-on-Don, Russia
2
Rostov State Medical University, Psychiatry department,
Rostov-on-Don, Russia
3
South Federal University, Genetics department, Rostov-on-Don,
Russia
∗
Corresponding author.
Introduction
Addiction to computer games (CA) is growing with
a lightning speed in whole world. Very few studies are focused in
the genetic basis of this disorder.
Objectives
To study the COMT and MAOA polymorphism in
addicts to computer games.
Methods
Totally 42 persons were included in this study, 22 of
them had CA and 20 were totally healthy. Out of 22 gamers, 10
persons had only CA. The rest of 12 patients suffered from another
psychiatric disorder besides of CA (Schizotypal disorder, depres-
sion, bipolar disorder). Their mean age was 16 years (15; 17) and
all of them were males.
Results
The total frequency of alleles 3R and 5R of MAOA gene
in patients with CA was 30.0%, which doesn’t have any statisti-
cal difference with the healthy persons. The genotype frequency
of Val158Met of COMT gene is high in CA rather than in healthy
persons (
2
= 6.85,
P
= 0.03). Also, the homozygotes Val are much
more in CA patients (59.1%) than in healthy persons (25%). On the
other hand, the Val/Met combination is lower in CA patients (18.2%)
than in healthy persons (55.0%).
Conclusion
The Val158Met polymorphism of gene COMT may
lead to CA formation.
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.921EV0592
Family-based association study
between the brain derived
neurotrophic factor (bdnf) gene and
the attention deficit hyperactivity
disorder in a Mexican population
J.P. Sánchez de la Cruz
1 ,∗
, A. López López
2, C.A. Tovilla Zárate
1,
R. Molina Sólis
2, A. Valencia Hernández
2, L. Gómez Valencia
2,
M.M. Rivera Angles
2, M.L. López Narváez
3,
D.Y. Bermúdez Oca˜na
1