Endocrine
Abstracts
May 2014 Volume 35
ISSN 1479-6848 (online)
16th European Congress of
Endocrinology 2014
3 –7 May 2014, Wrocław, Poland
published by
bioscientifica
Online version available at
www.endocrine-abstracts.org
Volume 35
May 2014
Endocrine Abstracts
16th European Congress of
Endocrinology
3–7 May 2014, Wrocław, Poland
EDITORS
The abstracts were marked by the Abstract Marking Panel selected by the Programme Organising Committee
ECE 2014 Programme Organising Committee
Paolo Beck-Peccoz
Anna Spada
Chair
Chair
Members
Max Bielohuby
Justo Castan˜o
Niki Karavitaki
Marta Korbonits
Krzysztof Kula
Agnes Linlart
Sten Lund
Valeriya Lyssenko
Andrej Milewicz
Efisio Puxeddu
Hans Romjin
Allan Vaag
Peter Varnai
M Donath Switzerland
J Drouin Canada
L Duntas Greece
G Eisenhofer Germany
S Farooqi UK
M Felicia Italy
A Ferlin Italy
C Follin Sweden
J Frystyk Denmark
L Fugazzola Italy
C Gaston UK
A-P Gimenez-Roqueplo France
E Gregoraszczu Poland
S Hahner Germany
N Hamdy Netherlands
T Hansen Denmark
TK Hansen Denmark
B Hemmingsen
A Hoeflich Germany
L Hofbauer Germany
P-M Holterhus Germany
E S Husebye Norway
A Januszewic Poland
N Jessen Denmark
D Jezova
A Juul Denmark
G Kahaly Germany
F Karpe UK
M Keil
F Kelestimur Turkey
RD Kineman USA
P King UK
ST Knudsen Denmark
M Korbonits UK
K Kula Poland
J Lenders Netherlands
NR Leslie UK
A Luger Austria
RM Luque Spain
M Luster Germany
M Manelli Italy
C Mathieu Belgium
J Mittag Sweden
J Newell-Price UK
M Niedziela Poland
S Nielsen Denmark
E Nieschlag Germany
P Nilsson Sweden
S Pearce UK
S Petersenn Germany
JR Petrie UK
M Pfeifer Sweden
V Pirags Latvia
A Pizzocaro Italy
D Power Portugal
PL Poulsen Denmark
M Puig Spain
S Radian UK
M Robledo Spain
C Ronchi Italy
M Rossini Italy
D Salvatore Italy
L Sa¨vendahl Sweden
N Skakkebaek Denmark
J Smit Netherlands
R Sustarsic
N Taylor UK
J Toppari Finland
M Toth
Z Toth
M Tzanela Greece
AJ Van der Lely Netherlands
J van Eck Netherlands
V Volke Estonia
J L Wemeau France
I Wilkinson UK
Z Wu Germany
P Yeoh UK
J Young France
L Zabuilene
MC Zatelli Italy
C Zillikens Netherlands
Abstract Marking Panel
A Agha Ireland
M Albiero
M Alevizaki Greece
MS Andersen Denmark
F Antoni
A Beckers Belgium
I Bernabeu Spain
J Bertherat France
F Beuschlein Germany
M Bidlingmaier Germany
M Blomberg-Jensen
Netherlands
J Bollerslev Norway
C Bousquet France
T Brue France
C Buchanan UK
F Cardona
J Castano Spain
P Chanson France
M Charalambous UK
B Chini Italy
I Chiondini Italy
L Chiovato Italy
MS Cooper Australia
L Czupryniak Poland
C Daousi UK
MT Dattani UK
W De Herder Netherlands
16th European Congress of Endocrinology 2014, Wrocław, Poland
SPONSORS
The ESE would like to thank its Corporate Members and the ECE 2014 sponsors
ECE Corporate Members
Eli Lilly
Ipsen
Laboratoire HRA Pharma
Merck Serono
Novartis Pharmacueticals
Novo Nordisk
Pfizer
Sandoz International Gmbh
ViroPharma SPRL
Gold Sponsors
Ipsen
Novartis
Bronze Sponsors
Alexion
ESE Office
Euro House
22 Apex Court
Woodlands
Bradley Stoke
Bristol BS32 4JT, UK
ECE 2014 Secretariat
Bioscientifica Ltd
Euro House, 22 Apex Court
Woodlands
Bradley Stoke
Bristol BS32 4JT, UK
Endocrine Abstracts (2014) Vol 35
Contact:
Tel:
Fax:
E-mail:
Web site:
Contact:
Tel:
Fax:
E-mail:
Website:
Andrea Davis
+44 (0)1454 642247
+44 (0)1454 642222
info@euro-endo.org
www.ese-hormones.org
Claire Arrigoni
+44 (0)1454 642240
+44 (0)1454 642222
conferences@bioscientifica.com
http://www.bioscientifica.com
16th European Congress of Endocrinology 2014, Wrocław, Poland
CONTENTS
16th European Congress of Endocrinology 2014
PRIZE LECTURES AND BIOGRAPHICAL NOTES
The European Journal of Endocrinology Prize Lecture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . EJE1
The Geoffrey Harris Prize Lecture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . GH1
PLENARY LECTURES
Genes, environment and endocrine disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Advances in molecular pathogenesis of thyroid cancer – therapeutic implications . . . . . . . . .
Good times, bad times: (patho)physiology of diurnal rhythms . . . . . . . . . . . . . . . . . . . .
Islet transplantation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Simultaneous treatment of menopausal symptoms and prevention of breast cancer: Is it possible?
Hypothalamic inflammation - cause or consequence of obesity? . . . . . . . . . . . . . . . . . . .
Reproduction and energy metabolism, an ancestral balance to be preserved for women’s health .
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PL1
PL2
PL3
PL4
PL5
PL6
PL7
Endocrine changes and treatment needs in critically ill patients . . . . . . . . . . . . . . . . . . . .
Pituitary development – from basic research to clinical practice . . . . . . . . . . . . . . . . . . . .
News from thyroid hormones: central transport, energy control and oxidative stress . . . . . . . .
Endocrine Nurses Session 1: Craniopharyngioma . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Obesity Beyond BMI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Focus on novel developments of PCOS - conclusions from the PCOS Task Force . . . . . . . . . . .
Nontumorous pituitary diseases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Membrane lipid composition and receptor function. Signalling and trafficking . . . . . . . . . . . .
EYES Session - Cold metabolic inflammation in obesity: ignored complication and treatment target?
Difficulties in the treatment of Graves’ orbitopathy . . . . . . . . . . . . . . . . . . . . . . . . . . .
Long term outcome of ‘cured’ pituitary patients . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Gut microbiota in diabetes and obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Endocrine Nurse Session 3: Meet the Nurse Expert - Management of Endocrine Emergencies . . . .
Clinical outcome of medical intervention in Disorder of Sex Development (DSD) . . . . . . . . . . .
Thromboembolism and contraception . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Metformin: old dog, new tricks . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Cushing’s syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Endocrine disease during pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Osteoporosis - An update . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
New hormones and endocrine tissues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Dilemmas in hormonal replacements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Novel therapies for thyroid cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Neuroendocrine tumours . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Nutrient regulation of metabolism and endocrine systems . . . . . . . . . . . . . . . . . . . . . . .
Gonadal hormones and obesity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Pitfalls in hormone measurement . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Brown Adipose Tissue . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Molecular pathophysiology for clinicians: receptor-related disorders . . . . . . . . . . . . . . . . . .
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. S1.1– S1.3
. S2.1– S2.3
. S3.1– S3.3
. S4.1– S4.3
. S5.1– S5.3
. S6.1– S6.3
. S7.1– S7.3
. S8.1– S8.3
. S9.1– S9.3
S10.1– S10.3
S11.1– S11.3
S12.1– S12.3
S13.1– S13.3
S14.1– S14.3
S15.1– S15.3
S16.1– S16.3
S17.1– S17.3
S18.1– S18.3
S19.1– S19.3
S20.1– S20.3
S21.1– S21.3
S22.1– S22.3
S23.1– S23.3
S24.1– S24.3
S25.1– S25.3
S26.1– S26.3
S27.1– S27.3
S28.1– S28.3
SYMPOSIA
Endocrine Abstracts (2014) Vol 35
16th European Congress of Endocrinology 2014, Wrocław, Poland
MEET THE EXPERT SESSIONS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . MTE1 –MTE17
ORAL COMMUNICATIONS
Thyroid clinical . . . . . . . . .
Adrenal Clinical . . . . . . . . .
Neuroendocrinology & Signalling
Diabetes and Obesity 1 . . . . .
Adrenal & Thyroid . . . . . . . .
Bone, Calcium & Vitamin D . . .
IGF-1 and Thyroid Basic . . . .
Pituitary Clinical . . . . . . . . .
Reproduction . . . . . . . . . . .
Endocrine Tumours . . . . . . .
Diabetes and Obesity 2 . . . . .
Pituitary Basic . . . . . . . . . .
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. . OC1.1– OC1.5
. . OC2.1– OC2.5
. . OC3.1– OC3.5
. . OC4.1– OC4.5
. . OC5.1– OC5.5
. . OC6.1– OC6.5
. . OC7.1 OC7.5
. . OC8.1– OC8.5
. . OC9.1– OC9.5
OC10.1 – OC10.5
OC11.1 – OC11.5
OC12.1 – OC12.5
NURSE POSTERS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . N1–N8
POSTER PRESENTATIONS
Adrenal cortex . . . . . . . . . . . . . . . . . . . .
Adrenal Medulla . . . . . . . . . . . . . . . . . . .
Bone and Osteoporosis . . . . . . . . . . . . . . .
Calcium and Vitamin D metabolism . . . . . . . .
Cardiovascular Endocrinology & Lipid Metabolism
Clinical case reports – Pituitary / Adrenal . . . .
Clinical case reports – Thyroid / Others . . . . . .
Developmental Endocrinology . . . . . . . . . . .
Diabetes (epidemiology, pathophysiology) . . . . .
Diabetes complications . . . . . . . . . . . . . . .
Diabetes therapy . . . . . . . . . . . . . . . . . . .
Endocrine disruptors . . . . . . . . . . . . . . . . .
Endocrine tumours and neoplasia . . . . . . . . .
Female reproduction . . . . . . . . . . . . . . . . .
Growth hormone IGF axis – basic . . . . . . . . .
Male reproduction . . . . . . . . . . . . . . . . . .
Neuroendocrinology . . . . . . . . . . . . . . . . .
Nuclear receptors and signal transduction . . . . .
Obesity . . . . . . . . . . . . . . . . . . . . . . . .
Paediatric endocrinology . . . . . . . . . . . . . .
Pituitary – Basic (Generously supported by IPSEN) .
Pituitary – Clinical (Generously supported by IPSEN)
Steroid metabolism and action . . . . . . . . . . .
Thyroid (non-cancer) . . . . . . . . . . . . . . . .
Thyroid cancer . . . . . . . . . . . . . . . . . . . .
INDEX OF AUTHORS
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. . . . P1– P56
. . . P57– P64
. . P65 – P100
. P101 – P168
. P169 – P209
. P210 – P260
. P261 – P332
. P333 – P339
. P340 – P402
. P403 – P461
. P462 – P501
. P502 – P513
. P514 – P613
. P614 – P667
. P668 – P683
. P684 – P708
. P709 – P735
. P736 – P739
. P740 – P792
. P793 – P825
. P826 – P836
. P837 – P945
. P946 – P957
. P958 –P1082
P1083 –P1152
16th European Congress of Endocrinology 2014, Wrocław, Poland
Poster Presentations
Endocrine Abstracts (2014) Vol 35
16th European Congress of Endocrinology 2014, Wrocław, Poland
P921
Increased prevalence of differentiated thyroid carcinoma in patients
with acromegaly
Andreea Serban1, Raluca Trifanescu1,2, Dan Niculescu1,2,
Mara Carsote1,2,1,2, Simona Galoiu1,2, Andrei Goldstein1 &
Catalina Poiana1,2
1
”C. I. Parhon’ National Institute of Endocrinology, Bucharest, Romania;
2
Carol Davila’ University of Medicine and Pharmacy, Bucharest, Romania.
Background
Acromegaly is associated with increased prevalence of thyroid diseases,
particularly of differentiated thyroid carcinoma.
Aim
To assess prevalence of thyroid diseases and thyroid cancer in patients with
acromegaly.
Patients and methods
Forty (10 M/30 F) acromegalic patients, 14 residents in iodine deficient areas,
aged 47G12.8 years, were retrospectively reviewed. Mean duration of
acromegaly was 7.6G9.5 years and median post diagnosis follow-up was 4.1
years. GH, IGF1 were measured by chemiluminescence (Liaison), TSH, FT4 by
immunometric assays (Immulite). Thyroid ultrasonography was performed in all
cases, thyroid scintigraphy was performed when indicated; fine needle aspiration
biopsy (FNAB) was performed in suspicious nodules, according to current
guidelines.
Results
Thyroid abnormalities were present in 28 patients (70%) in our series: diffuse
goiter in 8 patients (20%), simple nodular goiter in 5 patients (12.5%), nontoxic
multinodular goiter in 10 patients (25%), toxic multinodular goiter in 4 patients
(10%), Graves’ disease in one patient (2.5%); thyroid carcinoma was found in 3
patients (7.5%). Patients with thyroid nodules larger than 1 cm had significant
longer acromegaly duration (6.1G3.6 years) than patients without nodules or
nodules less than 1 cm (2.1G1.5 years), PZ0.008. Histological type in patients
with thyroid carcinoma was follicular variant of papillary thyroid carcinoma in all
three cases: 2 microcarcinomas and one macrocarcinoma. All three thyroid
carcinomas patients underwent total thyroidectomy and radioiodine treatment
(mean cumulative dose 181.7 mCi 131I) and were in stable remission.
Conclusion
Due to increased prevalence of differentiated thyroid carcinoma, active screening
for thyroid abnormalities is mandatory both in iodine sufficient and deficient
areas, especially in patients with longer duration of acromegaly.
DOI: 10.1530/endoabs.35.P921
P922
Oral and dental pathologies in patients with acromegaly
Ilonka Kreitschmann-Andermahr1,2, Johannes Kohlmann2, Daniel Starz2,
Sonja Siegel2, Sven Schlaffer2, Ursula Hirschfelder3, Rolf Buslei4 &
Michael Buchfelder2
1
Department of Neurosurgery, University of Essen-Duisburg, Essen,
Germany; 2Department of Neurosurgery, University of Erlangen-Nuremberg, Erlangen, Germany; 3Department of Orthodontics and Orofacial
Orthopaedics, University of Erlangen-Nuremberg, Erlangen, Germany;
4
Institute of Neuropathology, University of Erlangen-Nuremberg, Erlangen,
Germany.
Introduction
Growth of the tongue and mandible and dental pathologies are recognized
consequences of untreated growth hormone excess in acromegaly. However, data
on the frequency of the individual oro-dental pathologies are sparse. We,
therefore, developed a self-report questionnaire on typical oro-dental changes,
therapeutic measures, costs for prosthetic treatment and the role of dental
professionals in the diagnostic process of acromegaly.
Methods
The questionnaire was sent out to 320 patients with acromegaly, operated upon
between 2000 and 2012. 165 answers were received and analyzed statistically
with SPSS. Information on adenoma subtype was provided by the institute of
neuropathology.
Results
About 37% of all patients had visited a dentist at any time during the disease
process due to oro-dental pathologies. Most frequently, growth of the tongue
(54.5%), enlargement of interdental spaces (39.4%), mandibular growth (21.8%)
and mandibular prognatism (20%) were reported. 74.9% of the patients suffered
from an y oro-dental pathology and 9.6% reported these to be under the first selfnoticed symptoms. Seven patients were suspected to have acromegaly by the
dentist. The mean self-spent costs for prosthetic treatment amounted to 1,844V
Endocrine Abstracts (2014) Vol 35
(max. 18,000V). Of those patients with need for dental treatment 42.6% reported
a reduction of visits to the dentist after pituitary surgery. 67.9% of the patients
with proven acromegaly informed their dentist about their disease. While
adenoma subtype had no influence on the occurrence of oro-dental symptoms
(PZ0.816), their occurrence was significantly lower when acromegaly was
diagnosed and treated within 2 years from symptom onset (PZ0.007).
Conclusions
Our data show that oro-dental symptoms are frequent in patients with acromegaly
and incur frequent visits to dental health care providers. Since most of these
symptoms occur during the progressive, untreated course of the disease, we
suppose that an earlier diagnosis of acromegaly would reduce oro-dental
pathologies and result in lowered health care costs.
DOI: 10.1530/endoabs.35.P922
P923
Relationship between growth hormone deficiency and oxidative stress in
patients with heart failure: Preliminary data.
Antonio Mancini1, Sebastiano Raimondo1, Chantal Di Segni1,
Giovanni Gadotti1, Francesco Leo1, Carolina Ierardi2, Sonia Silvestri3,
Patrick Orlando3, Luca Tiano3 & Alfredo Pontecorvi1
1
Department of Medical Science, Division of Endocrinology, Catholic
University, Rome, Italy; 2Department of Cardiology, Catholic University,
Rome, Italy; 3Department of Clinical and Dental ScienceS, Polytechnic
University of Marche, Ancona, Italy.
It is well known that heart failure is associated with oxidative stress (OS).
Reactive oxygen species in fact influence sarcolemmal and mitochondrial ione
channels, which are responsible for cardiomyocyte excitability and are important
in myocardial remodeling after a myocardial infarction. The decrease of anabolic
axes can have a role in the progression of the illness.
In order to evaluate the relationship between growth hormone deficiency (GHD)
and indexes of OS, we have performed a dynamic GH evaluation and determined
oxidized form of coenzyme Q10 (CoQ10) (component of mitochondrial respiratory
chain also endowed with antioxidant properties) in a group of 12 patients (10 male
and 2 female, age 49–73) affected by heart failure (NYHA II-III; EF!40%).
GH secretion was evaluated after administration of Arginine (20 g/500 ml)C
GHRH (50 mg). Basal IGF1 was also assayed. GH was evaluated by CLIA
method, IGF1 by ECLIA and CoQ10 was evaluated by HPLC, as total and
oxidized form, also calculating their ratio (CoQox/CoQtot ratio).
Five out of 12 patients presented a total GHD (mean G ES peak GH: 3.87G
2.73 ng/ml; IGF1: 97.4G9.8 ng/ml). 3 showed a partial GHD (mean G ES peak
GH: 8.98G2.94 ng/ml; IGF1: 143G57.21 ng/ml). While 4 patients showed a
normal GH response (meanGES peak GH: 16.05G0.88 ng/ml; IGF1: 122.5G
24 ng/ml).
CoQox/CoQtot ratio were significantly higher in GHD patients (mean G ES 14G
0.04%) than in patients with normal GH (mean G ES 7G0.01%), thus expressing
an augmented oxidation of the molecule.
These preliminary data indicate that GHD is associated to an increased OS in
patients with heart failure and suggest that this hormonal alteration can have a role
in the physiopathology of this condition.
DOI: 10.1530/endoabs.35.P923
P924
GH Deficiency in HIV-infected patients compared to hypopituitary
patients
Chiara Diazzi1,2, Giulia Brigante1,2, Giulia Ferrannini1,2,
Giovanni Guaraldi3, Anna Ansaloni1,2, Manuela Simoni1,2 &
Vincenzo Rochira1,2
1
Unit an Chair of Endocrinology, Department of Biomedicine, Metabolism
and Neural sciences, University of Modena and reggio Emilia, Modena,
Italy; 2Department of Medicine, Endocrinology, Metabolism and Geriatrics,
Azienda AUSL of Modena, NOCSAE, Modena, Italy; 3Metabolic Clinic,
Infectious and tropical diseases Unit, Department of Medical and Surgical
Sciences for Children and Adults, University of Modena and reggio Emilia,
Modena, Italy.
Introduction
Growth Hormone deficiency (GHD) is frequent in patients with human
immunodeficiency virus 1 (HIV-1), undergoing highly active antiretroviral
therapy. GHD seems to depend on HIV-related lipodystrophy and to be less
frequent in women.
16th European Congress of Endocrinology 2014, Wrocław, Poland
Aim of the study
To investigate the association of gender, body composition and GH/IGF1 axis,
and to clarify whether GHD in HIV-infected patients is functional or a clinical
entity.
Methods
We compared 47 HIV-infected patients prospectively enrolled, with 36
hypopituitary subjects retrospectively selected reviewing record charts. We
evaluated basal serum GH, IGF1, GH peak and area under the curve (AUC) after
standard GH Releasing HormoneCArginine test; BMI, waist and hip
circumference and body composition by dual-energy X-ray absorptiometry
(DEXA). Data were analyzed by nonparametric Mann–Whitney test.
Results
HIV-infected patients had higher GH peak, AUC, and IGF1 (P!0.0001). BMI
(PZ0.003), total (P!0.0001) and trunk fat mass (PZ0.0003) were higher in
hypopituitary patients; waist to hip ratio (WHR) was higher in HIV-infected
patients (P!0.0001). GH peak was lower in hypopituitary men than women
(PZ0.001). Men showed higher WHR (PZ0.0082), total (PZ0.0002) and trunk
lean mass (PZ0.0008), while women had higher total (PZ0.0017) and trunk fat
mass (PZ0.0176). No gender differences were found in HIV-infected patients.
GH peak, AUC, and IGF1 were higher (P!0.0001) in HIV-infected than
hypopituitary men. No difference was found in women.
Conclusions
GHD seems to be worse in hypopituitary patients, suggesting that primary
pituitary disease affects GH/IGF1 axis more than HIV-1. Moreover, fat
distribution more than fat mass per se seems to affect GH/IGF1 axis in HIVinfected patients, since they have lower BMI but higher WHR. Furthermore, men
seem to have a worse deficit than women, suggesting a possible role of gender in
GH/IGF1 status. These differences could help distinguishing functional from
clinical GHD in HIV-infected subjects, and better targeting treatment strategies.
DOI: 10.1530/endoabs.35.P924
P925
Conservative management of pituitary apoplexy – own experience
Andrzej Styk1, Grzegorz Zielin´ski1, Przemysław Witek2 &
Andrzej Koziarski1
1
Department of Neurosurgery, Military Institute of Medicine, Warsaw,
Poland; 2Department of Endocrinology and Radioisotope Therapy, Military
Institute of Medicine, Warsaw, Poland.
Introduction
Pituitary apoplexy is a life-threatening entity developing as a result of ischemia or
hemorrhage into pre-existing pituitary tumor. Clinical course is characteristic and
commonly consists of severe headache accompanied by nausea, emesis, impaired
consciousness, visual field impairment as well as eyeballs movement restriction.
Symptoms are typically accompanied by secondary adrenal insufficiency.
Corticosteroids are drugs of choice regarding coexisting adrenal insufficiency.
In case of a lack of expected both general and neurological improvement during
conservative treatment, a surgery might be necessary. Prognosis in case of a
proper treatment is good.
Aim of the study was prospective evaluation of the results of conservative
treatment of pituitary apoplexy.
Material and methods
The analysis of seven patients (three women and four men) with diagnosed
pituitary apoplexy. Median age was 54 years old (range: 23 to 74 years). All
patients had endocrinological, ophthalmological and radiological assessment
performed before treatment as well as in the follow-up period.
Results
There were no fatal complications. Initial and distant hormonal assessment
revealed impairment of the anterior lobe of pituitary. In no cases diabetes
insipidus had been reported. During conservative treatment the visual field
improved as well as withdrawal of pre-existing paresis of ocular nerves were
obtained.
Conclusions
Conservative treatment is a safe method of pituitary apoplexy’s management.
DOI: 10.1530/endoabs.35.P925
P926
Pituitary apoplexy: surgical or conservative management
Duarte Sousa1, Olinda Marques2 & Rui Almeida3
Universidade do Minho, Braga, Portugal; 2Department of Endocrinoligy,
Hospital de Braga, Braga, Portugal; 3Department of Neurosurgery, Hospital
de Braga, Braga, Portugal.
1
Objectives
The rarity of pituitary apoplexy renders it a difficult subject for audit; hence there
are no evidence-based standards of optimum care for such patients. The main
controversy in management relates to the role of acute surgical intervention.
Recently, a more conservative management has been adopted towards patients
presenting with this condition. Therefore, it is important to evaluate the differences
in outcome between patients submitted to surgical and conservative management.
Methods
A retrospective analysis was performed to evaluate all patients that presented with
pituitary apoplexy since 1998 were followed in Hospital de Braga. Clinical
presentation, management, and clinical outcomes were evaluated. We then
performed a descriptive statistical analysis. Student’s t-test and Pearson’s c2 test
or Fisher’s exact test were used for comparing between groups. We admitted a P
value !0.05 to be statistically significant.
Results
There are no statistically significant differences in outcome between the patients
that had surgery and the patients that followed conservative management, (c2
(1)Z0.002; PZ0.967; nZ50). Differences of statistical significance were found
between the 2 groups in the following data: on average, the operated tumors are
11.67 mm bigger than the ones in patients with conservative management,
(t(48)Z4.925, P!0.001, dZ1.375, r2Z0.32); there are also differences in paraselar extension, (c2(4)Z16.554; PZ0.001; nZ50), and infra-selar extension,
(c2(2)Z7.935; PZ0.013; nZ50), with a bigger concentration of significant
results in Knosp 1 and Knosp 3. The surgical group also presented a bigger
concentration of growth into the sphenoidal sinus, (Adjusted Standardized
Residuals Oj1,96j).
Conclusion
The conservative management should be considered, without presenting an
increased risk for the patients, regardless of clinical presentation, visual deficits,
or endocrinal deficits during admission. However, we do recommend that patients
presenting with tendentially larger tumor diameter or Knosp should be evaluated
on a case-by-case basis in order to determine the best acute management.
DOI: 10.1530/endoabs.35.P926
P927
Histiocytosis of pituitary gland: a case report
Katarzyna Jankowska, Agnieszka Baranowska-Bik, Jan Bardadin &
Wojciech Zgliczyn´ski
Bielanski Hospital, Warsaw, Poland.
Histiocytosis is a disease caused by growth of histiocytes within one or more
organs. Symptomatology may be very different: from isolated skin or bone
lesions, by diabetes insipidus after life-threatening multisystem form. Diabetes
insipidus as a symptom of pituitary can be observed many years before visibility
of the changes in magnetic resonance imaging.
A case of 59-year-old woman who has experienced diabetes insipidus with no
other symptoms of hypopituitarism is presented in this study. It was the only
symptom of the disease. She felt very well and she didn’t receive any medical
treatment. Increased level of OB, LDH, and decreased urine specific gravity were
found in the laboratory tests. MRI of the pituitary revealed infiltration of the
hypothalamic- pituitary area. Extensive diagnostics was conducted to be sure that
inflammatory didn’t cause the infiltration. During this process, the presence of
numerous, multiorgan changes (numerous small focal lesions in the lung,
gallbladder, and ovaries) was revealed. Because of polyuria she received
desmopressin.
The most nagging discomfort the patient felt in the right ear. The ENT
consultation revealed a change resulting in narrowing of the external auditory
canal. The change within the right temporal bone was described during the CT of
the head. Material collected for histopathological examination during surgery
allowed for the diagnosis: eosinophilic granuloma. The inflammatory infiltration
was composed of lymphocytes and many histiocytes.
Owing to the high risk of complications, pituitary gland biopsy is not performed.
After inflammatory infiltration of the pituitary was excluded, histiocytosis of the
pituitary was recognized. The diagnose of the systemic histiocytosis was
performed and the patient was sent to chemotherapy.
DOI: 10.1530/endoabs.35.P927
Endocrine Abstracts (2014) Vol 35
16th European Congress of Endocrinology 2014, Wrocław, Poland
Author Index
Abaci, N P593
Abarikwu, S P708
Abbara, A OC3.1, OC9.4
& P617
Abbaszadegan, MR P108
Abdallah, NB P840
Abdelrazek, S P1041 &
P1055
Abdin, A P320 & P552
Abdollahi, M P405
Abdulla, H P848
Abeguile, G P148
Aberer, F P488
Aberle, J P581
Abeysinghe, P P786
Abi, A P472
Abouglila, K P846
Abrahamsson, N P770
Abraitiene, A P838
Abramavicius, S P369
Abreu, A P711
Abrosimov, AY P1108
Abs, R S21.3
Acar, B P343
Acar, FZ P1036 & P31
Acibucu, F P1120
Acikgoz, E P753
Ackermans, MT P946
Adamcova, M P22
Adamek, D P829
Adamidou, F P167
& P314
Adamska, A P134 & P663
Adamska, E OC4.1 & P776
Adas, G P14
Adas, M P14
Ademoglu, E P115
Adhiyaman, V P249
Adorini, L P696
Adukauskiene, D P931
Adversi, F P643
Ae Lee, K P1085
Aflorei, ED OC12.1
Afzal, N P1032
Agackiran, Y P136
Agapito, A P654 & P780
Agata, K P124
Agbaht, K P742
Aghaei, M P71
Aghajanova, Y P120 &
P477
Aghili, R P405
Agnieszka, C OC5.5
Aguiar, A P631
Aguilar-Diosdado, M
P206, P393, P395,
P398 & P496
Ahmed, A P1089
Ahmeti, I P248
Ahn, KJ P342 & P429
Aigelsreiter, A P192
Aimaretti, G P145
AiMin, X P771
Ajduk, M P785
Akc¸ay, G P66
Akbal, E P968
Akbay, E P270 & P271
Akcay, T P821
Akgul, OF P244, P245 &
P632
Akhtar, S P951
Akin, F OC9.5, P1027,
P263, P264 & P380
Akin, S P48 & P917
Akkurt, A P531
Akopyan, S P120
Akpinar, G P1010
Akpinar, S P275
Aksana, K P805
Aksoy, A P115
Aksyonova, E P778
Aktimur, R P126
Akturk, M P1030, P151,
P492 & P700
Akyildiz, M P171 & P172
Al-Dujaili, E P170
Al-Hayek, A P351
Al-Sabaan, F P351
Al-Saeed, A P351
Alacacioglu, A P332
Albarel, F P875
Alberiche, MdP P1073
Albersmeyer, M P868
Alborg, VC P909
Albrecht, E P739
Alebic, MS P686
Aled Rees, D OC5.2
Aleksandra, K OC5.5
Alesse, E P834 & P835
Alevizaki, M P1080 &
P1102
Alexander Iwen, K OC7.5
Alexandraki, K P537,
P598 & P608
Alexianu, M P815
Alexopoulou, O P860
Alfaro, JJ P467
Algu¨n, E P10
Alhumaidi, N P77
Ali Alhamza, AH P1
Ali Mansour, A P1
Ali, LA P542
Aliev, A P1050 & P584
Alikasifoglu, M P388
Alimova, N P358 & P417
Alkhalaf, F P77
Allelein, S P613
Allolio, B OC2.2, OC3.2,
OC5.3, P2, P533 &
P535
Almagro, RM P1002 &
P1003
Almanza, MR P909
Almeida, R P823, P926 &
P943
Almeida, T P654
Almomin, AMS P1
Alobedallah, A P351
Alonso, AA P575
Aloumanis, K P67 & P68
Alt-Tebacher, M P1042
Altas, A P1058
Altieri, B P535
Altinok, M P618
Altinova, A P446 & P492
Altinova, AE P1030 &
P151
Altun, B P968
Altunbas, HA P131, P74 &
P900
Altundal, N P894
Altunel, MS P432 & P433
Altunkaya, C P279 &
P285
Altunoren, O P238
Altuntas, Y P221 & P472
Alves, M P1009, P327,
P53, P546 & P547
Alves, MG P571
Alves, MR P702
Alves, R P461
Amani, MEA P984 & P985
Amar, L P49
Amaral, C P329, P457,
P764 & P769
Amaral, D P807
Amaral, FG P719
Amaro, T P1149
Ambroziak, U P338
Ammini, A P335
Ammini, AC P580 & P582
Amrani-Raissouni, T P106
Amselem, S P675
Amzar, D P543, P573 &
P893
Anaforog˘lu, P10, P23 &
P729
Anagnostis, P P167 &
P314
Anastasiu, D P65
Andersen, AS P337
Andersen, LLT P621
Andersen, M P618, P621
& P673
Andersen, MN OC1.2
Anderwald, C P129
Andrada, P P781
Andreas, B P714
Andreas, H P714
Andres, E P1042
Androulakis, I P641
Andrusiewicz, M P1119 &
P836
Andrysiak-Mamos, E
P100, P604 & P99
Andujar-Plata, P P731
Anelli, S P530
Angelini, F P937
Angelini, M S16.3
Angelopoulou, A P1102
Angelova, P P156
Anghel, GC P733
Anghel, R P734
Anheˆ, GF P719
Anil, C P403 & P468
Anna, S P180
Ansaloni, A P1053 &
P924
Ansari, NE P72
Antic, IB P299, P313,
P623, P624 & P625
Antic, S P828
Antiguedad, CG P445
Anton, M P814
Antonelou, M P920
Antosz, A P587
Antunes, A P823
Anwer, U P685 & P699
Aout, M P885 & P907
Apaydin, MA P863
Apollonatou, S P950
Apolloni, G P957
Apostolakis, M P1102
Arıkan, P958
Arau´jo-Vilar, D P811
Arabaci, E OC1.1
Aragu¨e´s, JM P350
Arakelyan, L P120
Aral, F P593
Aral, Y P385
16th European Congress of Endocrinology 2014, Wrocław, Poland
Regadera, J P738
Reghina, AD P431
Reimondo, G P8
Reincke, M MTE5, OC2.2,
OC5.4, P203, P37,
P564, P568 & P7
Reisch, N S14.1
Renata, C P1103
Rentziou, G P1102
Requena, JR P811
Requena, M P237 & P445
Rese´ndiz, KH P918
Resch, J OC7.5
Resmini, E OC12.5
Ress, C P861
Reyes-Garcı´a, R P91
Rezvani, R P773
Rheinheimer, J P365
Ribalta, MT P722
Ribeiro, C P1111
Riesco-Eizaguirre, G PL2
Ricciuti, A OC12.3
Richard, N P148
Richter-Unruh, A S14.1
Ricotti, R P145 & P27
Ridruejo, E P687
Ries, M P2
Rieske, P P97 & P98
Riester, A P37 & P568
Rigas, G P748
Rimpau, J P735
Rinaldi, E P47
Rinco´n-Ferna´ndez, D
P516
Rindi, G P549, P551 &
P578
Ripoll, RQ P909
Risbridger, G OC10.4
Ritvonen, E P881
Ritzel, K P7
Rivadeneira, L P237 &
P445
Rivera, NG P51 & P597
Rivera, R P741
Rivero-Corte´s, E OC12.2
Rivory, P P652
Rizoulis, A P1054
Rizvi, S P1031
Rizvi, SSR P1032, P685 &
P699
Roa, R P487
Roberts, J P914
Robledo, M P1095
Roca, M P500
Roca-Rodrı´guez, M P261
Roccio, M P27
Rochira, V P1053, P519,
P701, P924 & P955
Rodrı´guez Gutie´rrez, FJ
P1003
Rodrı´guez, C P1073
Rodrı´guez, E P1073
Rodrı´guez, JP P51 & P597
Rodrı´guez, R P322
Rodrı´guez-Medina, B
P695
Rodrı´guez-Molina, JM
P186
Rodrigues, D P1009,
P296, P325 & P327
Rodrigues, E P889
Rodrigues, P P17
Rodrigues, SC P719
Rodriguez, JP P498
Roemmler-Zehrer, J P735
Rogin´ska, D P54
Rogowicz-Frontczak, A
P378 & P420
Roine, R P881
Rojo-Martinez, G P789
Roma´n, MM P376
Romanelli, MMC P766
Romero, AO P743
Romero, MF P743
Romualdi, D P653
Ronchi, C OC2.3 & P533
Ronchi, CL OC2.2, OC5.3
& P535
Rosłonowska, E P557
Rosado, V P1095
Rosc, D P408
Rosca, R P204
Rosca, RI P529
Rosell, J P515
Rosenwald, A OC5.3
Roskosz, J OC1.5
& P1098
Roslon, M P1139
Ross, I P40
Ross, R P30 & P825
Ross, RJ OC5.2
Rossetti, P P1007
Rossetti, R P646
Rossi, M P692, P694 &
P704
Rossi, S P1126
Rostomyan, L P834
Roszak, M P1021
Rotermund, R P581
Rothenbuhler, A P140
Rotondi, S P834 & P835
Rousso, D P1047
Roux, A P652
Rozhinskaya, L P119, P24,
P730, P912, P919 &
P934
Rozhko, A P181
Rozkowszka, K P557
Ruas, L P1008, P1009,
P1111 & P296
Rubin, B P12 & P536
Rubino, M P128
Ruby, LCH P771
Ruchała, M P1035,
P1044, P1119, P202,
P338, P36, P836,
P982 & P983
Ruchala, M P326, P563,
P996 & S10.2
Rudnicka, M P99
Rudnik, A P832
Rudzinska, M P1131 &
P1135
Rudzki, G P254, P258 &
P556
Ruiz-Riquelme, A P811
Rupa, R P849
Ruprecht, Z P408
Rusak, M P776 & P818
Rusakov, V P266, P267
& P268
Rusalenko, M P181
Rusinek, D OC3.5 & P1152
Rusu, C P795, P814
& P819
Ruszkowska-Ciastek, B
P408
Ruszniewski, P P577
& P578
Rutishauser, J OC3.2
& P18
Rutkowska, A P511
Rutkowska, B P952
Rutter, M OC11.2
Ruvo, MD P831
Rybalchenko, V P422
Rybka, J P372
Rybka, W P372
Rydzanicz, M P338
Rymaszewska, J P127
& P930
Rys, A P157, P309 &
P777
Ryu, OH P384
Ryzhenkova, MI P1108
Sa´, J P389 & P390
Sa´daba, MC P669
Sa´nchez, A P1073
Sa´nchez, F P205
Sa´nchez, JRC P575
Sa´nchez, R P1073
Sa´nchez-Garcı´a, F P515
Sa´nchez-Iglesias, S P811
Sa´nchez-Zambrano, M
P205
Sa´sikova´, M P884
Se˛siadek, M P890
Słapa, R P557
Słoka, N P127
Słowin´ska-Srzednicka, J
P557
Sørensen, H P673
Sørensen, JA P621
Saad, F P478, P696, P754
& P755
Saaid, N P107
Saavedra, A P936
Sabino, T P654 & P780
Sabir, I P335
Sabt, A P77
Sacchi, S P639
Sacikara, M P136, P305,
P635, P980 & P987
Sadikova, E P142 & P375
Sadowski, T P160
Sadurska, E P1004
Sadykova, A P417 & P418
Saeger, W P901
Safari, R P71
Sag, S P753
Sagala, M P806
Saglam, F P1065, P305,
P421, P78 & P981
Sagliker, HS P231 & P301
Sahin, D P442
Sahin, F P69
Sahin, H P244 & P295
Sahin, I P1048 & P490
Sahin, M OC8.3, P139,
P146, P183, P228,
P230, P231, P238,
P244, P245, P295,
P301, P437, P5, P632,
P638 & P994
Saini, S P746
Saito, H P76
Sajardo, RB P575
Sajevets, T P277
Sajid, W P337
Sak, SD P61
Sakamoto, M P232 &
P897
Sakamoto, N P232
Saklamaz, A P171 & P172
Sala, E P845 & P898
Sala, GBL P643
Salam, R P107 & P959
Salas, MS P237 & P445
Salas-Salvado´, J S29.1
Salcuni, AS P81
Salgado, C P1149