

and aspirin 75
–
150 mg at the same time, concomitant consumption of
omeprazol and clopidogrel.
Key conclusions:
Due to the potential inappropriateness of pharma-
cological treatment among elderly the system of pharmaceutical care
in geriatrics seems to be one of the core element of healthcare system.
P-822
Colistin: an unknown adverse drug reaction in an elderly patient
E. Zafra, M. Martínez, W. López, A. Rodríguez.
Hospital Virgen del Valle
Introduction:
Interest in colistin use has increased dramatically in
recent times because of the emergence of bacterial strains resistant to
other clinically available antibiotics. Colistin has demonstrated an
excellent activity against various Gram-negative rod-shaped bacteria,
including multidrug-resistant Pseudomona aeruginosa, Acinetobacter
baumannii and Klebsiella pneumoniae.
Case report:
An 86 year-old male patient was medicated with
colistimethate sodium 2 MU/24 h (160 mg of colistimethate), adjust-
mented to renal function, because of an Acinetobacter baumannii
pneumonia, developing leukopenia (0.8 × 10^9/l) and neutropenia
(0.1 × 10^9/l) six days after treatment was began. Both were reversible
eleven days on discontinuation of treatment. No other treatments
were involved, and it was reported that the renal function did not get
worse. This unknowed adverse drug reaction was reported to the
Regional Pharmacovigilance Centre.
Conclusion:
Colistin became available for clinical use in the 1960s, but
was replaced in the 1970s with other antibiotics owing to its toxicity.
The optimal treatment dose according to the most recent pharmaco-
kinetic data for systemic infections in adults ranges widely between
240 and 720 mg daily in two or four divided doses. Nephrotoxicity and
neurotoxicity are the most common adverse effects. Toxicity is dose
dependent and reversible on discontinuation of treatment. Clinicians
should be careful about the adverse effect of colistin use. The
usefulness of colistin has been clearly documented and we believed
that colistin will be the
“
last line
”
therapeutic drug against Multiple-
Drug-Resistant Gram-negative pathogens in the 21st century.
P-823
Occurrence of a serotonin syndrome on escitalopramand tramadol
in a porphyria patient
M. Boulé
1
, M. Cloutier
1
, M. Waththuhew
1
, A. Lefevre-Fouach
1
, A. Proux
1
,
A. Zulfiqar
1
, J. Doucet
1
.
1
CHU de Rouen
Introduction:
Tramadol is associated with serotonin syndrome (SS), a
potentially lethal side effect, and is contraindicated in porphyria
patients. Here is the case of a porphyria patient that suffered SS
following tramadol administration. Case presentation: An 83 year-old
male with history of porphyria, depression, ischemic cardiopathy and
atrial fibrillationwas hospitalised for dyspnea and falls. His treatments
were escitalopram 10 mg, fluindione, pantoprazole, perindopril,
bisoprolol, spironolactone, rosuvastatin, paracetamol and furosemide.
January 19th: prescription and administration of one dose of tramadol
extended-release 100 mg, no escitalopram received. January 20th: he
presented clonic seizures without loss of consciousness, postictal
state, drowsiness, myoclonic seizures, stiffness, Babinski signs and
fever. SS was suspected. Escitalopram and tramadol were discon-
tinued. Provided care was active surveillance, EEG and CT scan.
Complete symptom resolution occurred by January 22th.
Key conclusions:
The association of escitalopram and tramadol led to
a SS. Tramadol introduction was the only treatment modification prior
to symptoms. Although he did not receive escitalopram on January
19th, its half-life of 30 hours meant that it could still interact with
tramadol. Fast recovery at drug discontinuation increased the
iatrogenic suspicion. The patient did not experience any porphyria
crises even though he received different treatments that could have
triggered one (tramadol, spironolactone and IV paracetamol). They
were discontinued on January 20th. Considering the symptoms began
after a standard dose of tramadol, it is likely that its interaction with
escitalopram was responsible for the SS. It is not possible to confirm
the increased susceptibility of SS in porphyric patients due to a lack of
data.
P-824
Consequences of the angiotensin-converting-enzyme inhibitors
on kidneys in high-risk elderly patients
A. Lefèvre Fouache
1
, M. Waththuhewa
1
, A.A. Zulfiqar
1
, R. Bolis
1
, A. Jego
1
,
B. Heurtaux
1
, M. Boulé
1
, M. Cloutier
1
, J. Doucet
1
.
1
CHU de Rouen, Rouen,
France
Introduction:
Many medicines are nephrotoxic. Among them,
angiotensin-converting-enzyme inhibitors (ACEI) are known to
induce functional acute renal failure (ARF). They are widely used in
geriatric population.
Methods:
Here is a case of an ACEI-induced nephropathy aggravated
by left-kidney artery thrombosis and right-kidney artery stenosis.
Context:
A 90 year-old female patient with history of hypertension
and transient ischemic attack, was hospitalized for an acute degrad-
ation of general state. Biological tests were normal and renal clearance
was at 47 mL/min. Due to hypertension, ramipril was prescribed at
5 mg and reported well tolerated beforehand. She was transferred to
after-care where the patient experienced nausea and vomiting.
Discovery of an acute renal failure with renal clearance at 17 mL/min.
Digoxin and ramipril were discontinued. RC degradation at 9 mL/min
led to dialysis sessions. The echography revealed
“
normal kidneys
”
.
Pharmacovigilance experts imputed the functional ARF to ramipril
with one similar case reported in France. The Doppler ultrasound
showed a left-kidney artery thrombosis and a right-kidney artery
stenosis. Progressive improvement followed with RC at 13 mL/min on
25/03.
Key conclusions:
We identified avoidable mistakes: No biologic
monitoring at ramipril initiation nor the following 11 days despite
patient transfer No pharmaceutical analysis Non-avoidable mistakes
and contributory factors include: Potentially nephrotoxic drugs have
been administrated before discovery of the nephropathy Old, diabetic
and dehydrated patient No recommendation on systematic nephro-
pathy research by imaging at ACEI initiation Many contributory factors
and malfunctions led to this incident with important consequences. It
is important to follow recommendations on nephrotoxic drug
monitoring in high risk patients.
P-825
Duodenal ulcer perforation linked to long-term nicorandil-
acetylsalicylic acid association
B. Heurtaux
1
, M. Waththuhewa
1
, A.A. Zulfiqar
1
, A. Hoffmann
1
,
E. Delbende
1
, S. Quitadamo
1
, A. Lefèvre Fouache
1
, A. Proux
1
, J. Doucet
1
.
1
CHU de Rouen
Introduction:
Duodenal ulcer (DU) is a disease affecting 8% of the
active population and its incidence has been decreasing in the past
years. The most well-known drug causing DU are NSAIDs. Here is the
case of a patient suffering from a duodenal bulb perforation (DBP)
while being treated by acetylsalicylic acid (AA) and nicorandil, also
known to worsen DU.
Context:
A 93 year-old woman was admitted for a confusional
syndrome. Her medical history include Alzheimer
’
s disease, hyper-
cholesterolemia, high blood pressure and acute coronary syndrome
(ACS) in 2003 with the introduction of AA 160 mg and nicorandil
10 mg. Between 2012 and 2014, omeprazole (proton pump inhibitor,
PPI) was started for epigastric pain. In February 2016, she was
hospitalised for a generalised peritonitis due to a DBP. One month
later, she was hospitalised and a recurrence of DU was suspected,
which justified nicorandil discontinuation. Gastric disorders were
resolved thirty days later.
Key conclusions:
The patient may have experienced two occurrences
of DU. Nicorandil-AA long-term association probably led to a DBP, a
serious and rare DU complication. ACS history meant that AA
’
s risk-
benefit ratio was in favour of its maintenance. Considering that
nicorandil-only discontinuation led to symptoms resolution, it is likely
Poster presentations / European Geriatric Medicine 7S1 (2016) S29
–
S259
S246