

25th European Congress of Psychiatry / European Psychiatry 41S (2017) S106–S169
S163
brain regions. Empirical evidence suggests that these functions are
altered in schizotypy, which is thought to reflect the subclinical
expression of the symptoms of schizophrenia in the general pop-
ulation. A number of clinical studies reported that interpersonal
interaction and social stimulation have an impact on the onset and
progress of schizophrenia.
Objectives
We conducted a study on personal space in a sample
of student screened for schizotypal traits using a paradigm that was
not affected by emotional and social interference.
Aims
The aimwas to evaluate the relationship between personal
space and schizotypy traits.
Methods
Thirty-four subject recruited for the study completed
the Schizotypal Personality Questionnaire (SPQ). According to the
SPQ results participants were splitted into two groups (High, Low).
Each participant performed a PeriPersonal Space (PPS) task.
Results
Our results show a more extended boundary of the
peripersonal space in people with high schizotypy compared to
people with low schizotypy even without emotional and social
interference.
Conclusions
People with high traits of schizotypy suffer from a
difficulty in social integration because of being unable to adapt
the social behavior. A better understanding of the mechanisms
for abnormal interactive behavior could provide significant valid
guidelines for innovating insertion programs that aims to improve
social functioning.
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.2041EW0173
Poor CYP2D6 and ultrarapid CYP2C19
metabolizer: Clinical challenge in
psychiatric treatment
E. Dlugauskas
1 ,∗
, A . Lengvenyte
2 , R. Strumila
3 , A.Utkus
41
Vilnius University, Clinic of Psychiatry, Center of Neurology,
Departament of Psychiatry, Departament of Psychiatry, Vilnius,
Lithuania
2
Vilnius University, Faculty of Medicine, Clinic of Psychiatry, Vilnius,
Lithuania
3
Vilnius University, Faculty of Medicine, Faculty of Medicine, Vilnius,
Lithuania
4
Vilnius University, Department of Human and Medical Genetics,
Center for Medical Genetics, Vilnius, Lithuania
∗
Corresponding author.
Introduction
Finding the right medication in psychiatry can be
very demanding both for the doctor and for the patient. It becomes
extremely gruelingwhen the patient has a rare type ofmetabolizing
enzymes, and many drugs may be ineffective or cause side effects.
Objectives
To highlight the therapeutic difficulties in psychiatric
treatment of the patient with complex genetic cytochrome P450
system alterations.
Aims
To provide an example on a complicated treatment course
of the patient that is poor CYP2D6 and ultrarapid CYP2C19 metab-
olizer.
Methods
Literature review in scientific database–Pubmed–and
case report presentation.
Results
We report a case of a woman in her early twenties who
was repeatedly referred for psychiatric treatment. A diagnosis of
paranoid schizophrenia was established, but all treatment rounds
were unsuccessful, the illness kept progressing, and major depres-
sive disorder aggravated the clinical picture. The patient became
suicidal and injured herself. During the sixth hospitalization in
one year the CYP2D6, CYP2C19 and CYP2C9 genotyping was done.
CYP2C19 ultrarapid (*1/*17) and CYP2D6 poor metabolizer (*4/*5)
profile was discovered. Drugs, that should have been avoided due
to the patient’s genetic profile, had been prescribed throughout five
hospitalizations in a row.
Conclusions
As ultrarapid CYP2C19 metabolizers compose
around 3–4% and poor CYP2D6–6–10% of Caucasians, this case
presents a rare genetic variant that only 0.18–0.4% of Caucasian
population may have. These cases can be extremely clinically
challenging and affect healthcare outcomes and costs. Further
studies that would include clinical effectivity, drug concentration
and genetic testing results are needed.
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.2042EW0174
Insight gained from genome-wide
interaction and enrichment analysis
on weight gain during citalopram
treatment
H. Corfitsen , A. Drago
∗
Psykiatrisk Forskningsenhed Vest, Department of Clinical Medicine,
Aarhus University, Herning, Denmark
∗
Corresponding author.
Introduction
Weight gain is a side effect of pharmacological
antidepressant treatments, causing a poorer compliance, increas-
ing the risk of metabolic syndrome and periods of untreated
disease.
Objectives
The ability to precisely prescribe pharmacological
treatments based on personal genetic makeups would increase the
quality of the current antidepressant treatments.
Aims
The molecular pathways enriched during citalopram
induced weight gain are identified.
Methods
643 depressed citalopram treated individuals with
available clinical and genome-wide genetic information were
investigated in the present contribution in order to identify the
molecular pathways that holds the key to weight gain. Statistics
were conducted in R environment (Bioconductor and Reactome
packages), ANOVA and MANCOVA served when appropriate. Plink
was used for genetic analysis in a linux environment.
Results
One hundred and eleven individuals had their weight
increased after treatment with citalopram. The axon guidance
(
P
. adjust = 0.005) and the developmental biology pathway (
P
.
adjust = 0.01) were found to be enriched in genetic variations asso-
ciated with weight gain.
Conclusions
The development biology pathway includes molec-
ular cascades involved in the regulation of beta-cell development,
and the transcriptional regulation of white adipocyte differenti-
ation. A number of variations were harboured by genes whose
products are involved in the synthesis of collagen (
COL4A3
,
COL5A1
and
ITGA1
), activity of the thyroid-hormones (
NCOR1
and
NCOR2
),
energy metabolism (
ADIPOQ
,
PPARGC1A
) and myogenic differenti-
ation (
CDON
). A molecular pathway analysis conducted in a sample
of depressed patients identifies new candidate genes whose future
investigation may grant relevant insights in the molecular events
that drive weight gain during antidepressant treatment.
Disclosure of interest
The authors have not supplied their decla-
ration of competing interest.
http://dx.doi.org/10.1016/j.eurpsy.2017.01.2043EW0175
Predicting antidepressant response
from genes
H. Corfitsen , A. Drago
∗
Psykiatrisk Forskningsenhed Vest, Department of Clinical Medicine,
Aarhus University, Herning, Denmark
∗
Corresponding author.
Introduction
Pharmacogenetics may inform an accurate pre-
scribing of antidepressants by identifying the genetic background