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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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 . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 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
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