Læknablaðið - 15.09.2006, Side 63

UMRÆÐA & FRÉTTIR / DOKTORSVÖRN
Nýr doktor í geðlækningum
Þann 25. maí síðastliðinn varði Páll Matthíasson
geðlæknir doktorsritgerð sína við Geðfræðastofnun
Lundúnaháskóla (Institute of Psychiatry,University
of London). Handleiðarar voru Prófessor Robert
W. Kerwin, Institute of Psychiatry og Dr. Michael
J. Travis, University of Pittsburg. Andmælendur
voru Prófessor Thomas R. Barnes frá Imperial
College, University of London og Prófessor Sean
Spence frá University of Sheffield. Titill ritgerð-
arinnar var: Dealing with treatment resistance to
clozapine: Characteristics of treatment response in
schizophrenia. Hér á eftir fer ágrip ritgerðarinnar
á ensku:
Páll fæddist í Reykjavík árið 1966 og eru for-
eldrar hans Matthías Guðjónsson verslunarmað-
ur og Guðrún Guðjónsdóttir kennari. Hann
útskrifaðist úr Menntaskólanum í Reykjavík
1986 og lauk embættisprófi frá læknadeild
Háskóla íslands 1994. Hann lauk sérfræði-
prófi í geðlækningum frá Maudsleyspítalanum
í Lundúnum og starfar nú sem yfirlæknir á The
Huntercombe Hospital-Roehampton þar í borg,
jafnframt því að stunda áfram rannsóknir við
Geðfræðastofnun Lundúnaháskóla. Páll er kvænt-
ur Olöfu Björnsdóttur myndlistarmanni og eiga
þau tvö börn, Valdemar og Júlíu.
Dr. Páll Matthíasson
geðlæknir
Background:
Clozapine, the treatment of choice in treatment-resistant
schizophrenia, is not effective in up to half of patients.
Aims of this thesis were: to verify whether clozapine
augmentation with amisulpride, an atypical antipsychotic
with preferential affinity at dopaminergic D2-like receptors,
is clinically effective; to test the prediction that changes
in D2—like receptor availability might explain that
improvement; to explore clinical and receptor availability
characteristics of good clozapine responders.
Methods:
Study 1: Thirty-three patients with schizophrenia, partially
or non-responsive to clozapine, had augmentation with
amisulpride using an open label design.
Study 2: Ten patients recruited from study 1 underwent
1231-IBZM SPET scans at baseline and after 10-12 weeks
on amisulpride augmentation, to assess striatal D2—like
receptor binding potential. Ten matched controls had one
1231-IBZM scan. Scanning was carried out using a Picker
Prism 3000XP triple headed SPET camera.
Study 3: Ten “good” responders to clozapine monotherapy
were matched to patients in study 2 and had one 1231-
IBZM scan.
Results:
Study 1: Twenty-eight subjects (85%) completed 6
months’ augmentation. There was a statistically significant
improvement from baseline in clinical rating scales and no
change in side-effects. 71% and 32% of patients showed
a 20% and 50% reduction in BPRS respectively.
Study 2: Patients had mean striatal D2—like receptor
occupancy of 47% at baseline, which increased with
amisulpride augmentation to 59%.
Study 3: Clozapine responders were on much lower doses
of clozapine (331 mg/day) with lower s-clozapine levels
(0.26 ng/L). Their D2-like occupancy was 45%.
Conclusion: The augmentation led to substantial
improvement in both positive and negative symptoms
and was well tolerated. It raised D2-like binding to likely
“threshold levels” for response. Some patients require
both the broad receptor occupancy profile of clozapine
and a higher degree of D2—like receptor occupancy than
can be provided by clozapine alone.
Læknablaðið 2006/92 643