European Psychiatry - Volume 41 - April 2017

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S802 25th European Congress of Psychiatry / European Psychiatry 41S (2017) S772–S846
suggests that HE is an autoimmune disorder instead of thyroid dis-
ease.
Disclosure of interest The author has not supplied his/her decla-
ration of competing interest.
EV1218
Brain metabolic abnormalities in
schizophrenia patients
M. Amorim ∗ oreira arques ummavielle
1 School of Allied Health Technologies of the Polytechnic Institute of
Porto, Clinical Analysis and Public Health, Vila Nova de Gaia, Portugal
2 School of Allied Health Technologies of the Polytechnic Institute of
Porto, LabRP, Vila Nova de Gaia, Portugal
3 I3S consortium, University of Porto, Addiction Biology Group, Porto,
Portugal
∗ Corresponding author.
Introduction Main schizophrenia symptoms result from abnor-
malities in brain function, such as hypofrontality and structural
deficits on the prefrontal-thalamic-cerebellar circuit, as shown
in brain imaging studies in first-episode SCZ patients. Whether
metabolic alterationsmay be underlying these events is being stud-
ied thoroughly.
Objectives/aims To assess brain metabolic disturbances in first
episode and/or drug-naïve SCZ patients.
Methods We conducted a literature review through Pubmed
search for MeSH: schizophrenia, metabolism, glucose, insulin,
brain. Controlled studies on first episode and/or drug-naïve SCZ
patients were included.
Results Lower metabolic activity in the frontal regions of the
brain is associated to an increase in norepinephrine transmis-
sion and decrease in dopaminergic transmission with reduced
dopamine efflux in the frontal cortex. This seems to lead to cel-
lular changes resulting in resulting lower blood flow and glucose
demand. Molecular analysis of postmortemSCZ patients’ brains has
indicated alterations in glucose metabolism and insulin signalling
pathways, showing evidence for prefrontal cortex decreased
expression of glucosemetabolism, namely glycolytic enzymes such
as glyceraldehyde 3-phosphate dehydrogenase, hexokinase, phos-
phoglycerate mutase, enolase and pyruvate kinase and decreased
levels and phosphorylation of the insulin receptor and insulin
signalling proteins AKT1 and GSK3 . Significantly elevated glu-
cose concentrations in cerebrospinal fluid were observed in SCZ
patients, but with no serum levels differences. A SCZ brain specific
increased glucose could be explained by preferential utilization of
lactate, predominantly produced by astrocytes, over glucose as an
energy substrate.
Conclusions Abnormalities in brain glucose metabolism and
insulin signalling seem to appear in early stages of SCZ, suggesting
a role in SCZ onset and pathophysiology.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
EV1219
Peripheric metabolic abnormalities in
schizophrenia patients
M. Amorim ∗ oreira arques ummavielle
1 School of Allied Health Technologies of the Polytechnic Institute of
Porto, Clinical Analysis and Public Health, Vila Nova de Gaia, Portugal
2 School of Allied Health Technologies of the Polytechnic Institute of
Porto, LabRP, Vila Nova de Gaia, Portugal
3 i3S consortium, University of Porto, Addiction Biology Group, Porto,
Portugal
∗ Corresponding author.
Introduction Schizophrenia (SCZ) is frequently associated with
metabolic symptoms including dyslipidaemia, hyperinsulinemia,
type 2 diabetes and obesity. In fact, SCZ patients have been reported
to present higher prevalence of these conditions than general
population, commonly associated to second generation antipsy-
chotic therapy. Recent studies, however, have demonstrated that
peripheral metabolic disturbances can appear at disease onset or
drug-naïve patients.
Objectives/aims To assess metabolic disturbances in first episode
and/or drug-naïve SCZ patients.
Methods We conducted a literature review through Pubmed
search for MeSH: schizophrenia, metabolism, glucose, insulin. Con-
trolled studies on first episode and/or drug-naïve SCZ patients were
included.
Results Several studies showed no change in SCZ patients’ fas-
ting blood glucose, while others found increased glucose levels and
impaired glucose tolerance in SCZ patients compared to healthy
controls in several recent studies. Hyperinsulinemia and insulin
resistance have also been identified in antipsychotic-naïve SCZ
patients and it has been suggested that early onset patients are
more likely to present insulin resistance. In addition, there’s evi-
dence of increased circulating levels of chromogranin A, pancreatic
polypeptide, prolactin, cortisol, progesterone, thus emphasising
that multiple components of the hypothalamic-pituitary-adrenal-
gonadal axis may be affected in SCZ. These elevations were
associated to normal glycaemia suggesting there may be insulin
intolerance during early stages of SCZ, requiring an increased secre-
tion from pancreatic Bcells to maintain normal glucose levels.
Conclusions Recent studies of first onset and/or drug-free
schizophrenia patients have shown impaired fasting glucose tol-
erance, hyperinsulinemia and insulin intolerance, suggesting that
metabolic abnormalities may play a role in SCZ onset and patho-
physiology.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
EV1220
Systemic review: High dose
olanzapine treatment for treatment
resistant schizophrenia
Z. Azvee ∗, J. Lally
1 Beaumont Hospital, Liaison Psychiatry, Dublin, Ireland
2 Royal College of Surgeons Ireland, Psychiatry, Dublin, Ireland
∗ Corresponding author.
Objectives Schizophrenia is a major mental illness with a
progressive course. Thirty percent of cases of patients with
schizophrenia do not respond to adequate trials of at least 2 dif-
ferent groups of antipsychotics,are currently classified as having
treatment resistant schizophrenia (TRS). Clozapine remains the
gold standard, treatment of choice for TRS. However, clozapine does
not come without its own challenges. Its risk profile, particularly
agranulocytosis, reported in 1% of cases, has led to the necessity
of weekly blood counts within the first 18 weeks of treatment
and subsequently every month with slow dose titration. Clinically,
sedation, weight gain and hypersalivation may further hamper
the compliance of patients. Non-compliance has been reported to
cause rebound psychosis. Recent studies have raised questions as
to which antipsychotic is most efficacious for TRS. Thus, we con-
ducted a systematic review of high dose olanzapine treatment for
people with TRS.
Method A systematic review of prospective studies found
through search of PubMed, Scopus and hand-searched key papers
which included randomized controlled trials and open-label stud-
ies which looked at high dose of olanzapine treatment response for
TRS.