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Angelica Sharma Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Katharine Lazarus Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Deborah Papadopoulou Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Hemanth Prabhudev Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Tricia Tan Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, North West London Pathology, London, UK

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Karim Meeran Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Sirazum Choudhury Division of Diabetes, Endocrinology and Metabolism, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, North West London Pathology, London, UK

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mortality ( 2 ). Replacement with glucocorticoid therapy is the mainstay of treatment, with an objective to mimic the circadian cortisol profile ( 3 ). Current guidelines recommend the use of hydrocortisone in divided doses or low-dose (3–5 mg

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Sandra R Dahl Hormone Laboratory, Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway

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Ingrid Nermoen Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Division of Medicine, Akershus University Hospital, Lørenskog, Norway

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Ingeborg Brønstad National Centre for Ultrasound in Gastroenterology, Haukeland University Hospital, Bergen, Norway
Department of Clinical Medicine, University of Bergen, Bergen, Norway

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Eystein S Husebye Department of Clinical Science, University of Bergen, Bergen, Norway
K.G. Jebsen-Center for Autoimmune Diseases, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Kristian Løvås Department of Clinical Science, University of Bergen, Bergen, Norway
K.G. Jebsen-Center for Autoimmune Diseases, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Per M Thorsby Hormone Laboratory, Department of Medical Biochemistry, Oslo University Hospital, Oslo, Norway

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Introduction Congenital adrenal hyperplasia (CAH) is a group of autosomal recessive disorders with impaired biosynthesis of adrenal glucocorticosteroids and defects in cortisol biosynthesis. More than 95% of cases are caused by mutations in

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Ali Abbara Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK

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Sophie Clarke Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK

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Pei Chia Eng Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK

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James Milburn Imperial College Healthcare NHS Trust, London, UK

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Devavrata Joshi Imperial College Healthcare NHS Trust, London, UK

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Alexander N Comninos Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK
Imperial College Healthcare NHS Trust, London, UK

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Rozana Ramli Imperial College Healthcare NHS Trust, London, UK

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Amrish Mehta Imperial College Healthcare NHS Trust, London, UK

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Brynmor Jones Imperial College Healthcare NHS Trust, London, UK

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Florian Wernig Imperial College Healthcare NHS Trust, London, UK

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Ramesh Nair Imperial College Healthcare NHS Trust, London, UK

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Nigel Mendoza Imperial College Healthcare NHS Trust, London, UK

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Amir H Sam Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK
Imperial College Healthcare NHS Trust, London, UK

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Emma Hatfield Imperial College Healthcare NHS Trust, London, UK

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Karim Meeran Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK
Imperial College Healthcare NHS Trust, London, UK

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Waljit S Dhillo Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK
Imperial College Healthcare NHS Trust, London, UK

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Niamh M Martin Department of Investigative Medicine, Imperial College London, Hammersmith Hospital, London, UK
Imperial College Healthcare NHS Trust, London, UK

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(persistent hiccup). One patient was hypotensive (systolic BP <90 mmHg; serum cortisol of 118 nmol/L and serum sodium of 115 nmol/L on admission). However, 11/30 were hypertensive at presentation (systolic BP >140 mmHg) ( Table 2 ). Symptoms consistent with

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Peter Ergang Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Anna Mikulecká Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Martin Vodicˇka Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic

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Karla Vagnerová Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Ivan Mikšík Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic

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Jirˇí Pácha Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Department of Physiology, Faculty of Science, Charles University, Prague, Czech Republic

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-hydroxysteroid dehydrogenase type 1 (11HSD1) and type 2 (11HSD2). 11HSD2 is an enzyme that catalyzes the oxidations of cortisol and corticosterone to the inactive cortisone and 11-dehydrocorticosterone, reducing the local glucocorticoid signals. In contrast, 11HSD1 converts

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Paal Methlie Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Steinar Hustad Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Ralf Kellman Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Bjørg Almås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Martina M Erichsen Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Eystein S Husebye Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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Kristian Løvås Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway
Department of Clinical Science, Department of Medicine, University of Bergen, N-5021 Bergen, Norway

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monitoring of prednisone and prednisolone has the potential to optimize treatment (11, 12) . Because of the widespread use of these glucocorticoids and impact on endogenous cortisol levels, information on serum levels may also be valuable in the setting of a

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Gavin P Vinson School of Biological and Chemical Sciences, Queen Mary University of London, London E1 4NS, UK

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Caroline H Brennan School of Biological and Chemical Sciences, Queen Mary University of London, London E1 4NS, UK

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actually represent a drive to lower cortisol, with its sequelae? Or is the heightened secretion of corticosteroids in drug withdrawal simply a response to stress? We here argue that the adrenal cortex has a critical role in the acquisition of addiction and

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Solène Castellnou Service d’Endocrinologie, Centre de Référence des Maladies Rares de l’Hypophyse HYPO, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France
Université Lyon 1, Villeurbanne, France

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Alexandre Vasiljevic Université Lyon 1, Villeurbanne, France
Centre de Biologie et Pathologie Est, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France
INSERM U1052, CNRS, UMR5286, Centre de Recherche en Cancérologie de Lyon, Lyon, France

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Véronique Lapras Service de Radiologie, Centre Hospitalier Lyon Sud, Hospices Civils de Lyon, Pierre-Bénite, France

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Véronique Raverot Laboratoire d’Hormonologie, Centre de Biologie et Pathologie Est, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France

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Eudeline Alix Département de Cytogénétique, Centre de Biologie et Pathologie Est, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France

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Françoise Borson-Chazot Service d’Endocrinologie, Centre de Référence des Maladies Rares de l’Hypophyse HYPO, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France
Université Lyon 1, Villeurbanne, France

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Emmanuel Jouanneau Université Lyon 1, Villeurbanne, France
INSERM U1052, CNRS, UMR5286, Centre de Recherche en Cancérologie de Lyon, Lyon, France
Service de Neurochirurgie, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France

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Gérald Raverot Service d’Endocrinologie, Centre de Référence des Maladies Rares de l’Hypophyse HYPO, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France
Université Lyon 1, Villeurbanne, France
INSERM U1052, CNRS, UMR5286, Centre de Recherche en Cancérologie de Lyon, Lyon, France

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Hélène Lasolle Service d’Endocrinologie, Centre de Référence des Maladies Rares de l’Hypophyse HYPO, Groupement Hospitalier Est, Hospices Civils de Lyon, Bron, France
Université Lyon 1, Villeurbanne, France
INSERM U1052, CNRS, UMR5286, Centre de Recherche en Cancérologie de Lyon, Lyon, France

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Introduction Cushing’s disease is a rare disorder defined as chronic hypercortisolism due to a corticotropin-secreting pituitary tumor (corticotroph tumor) ( 1 ). Chronic cortisol excess is responsible for multisystem morbidity, contributing

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Lia Ferreira Department of Endocrinology, Centro Hospitalar do Porto, Porto, Portugal

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João Silva Department of Endocrinology, Hospital das Forças Armadas, Lisboa, Portugal

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Susana Garrido Department of Endocrinology, Centro Hospitalar Tâmega e Sousa, Porto, Portugal

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Carlos Bello Department of Endocrinology, Centro Hospitalar Lisboa Ocidental, Lisboa, Portugal

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Diana Oliveira Department of Endocrinology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal

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Hélder Simões Department of Endocrinology, Instituto Português de Oncologia de Lisboa Francisco Gentil, Lisboa, Portugal

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Isabel Paiva Department of Endocrinology, Centro Hospitalar e Universitário de Coimbra, Coimbra, Portugal

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Joana Guimarães Department of Endocrinology, Centro Hospitalar do Baixo Vouga, Aveiro, Portugal

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Marta Ferreira Department of Endocrinology, Centro Hospitalar de Leiria, Leiria, Portugal

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Teresa Pereira Department of Endocrinology, Centro Hospitalar de Leiria, Leiria, Portugal

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Rita Bettencourt-Silva Department of Endocrinology, Centro Hospitalar de São João, Porto, Portugal

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Ana Filipa Martins Department of Endocrinology, Centro Hospitalar Lisboa Norte, Lisboa, Portugal

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Tiago Silva Department of Endocrinology, Hospital Garcia da Orta, Lisboa, Portugal

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Vera Fernandes Department of Endocrinology, Hospital de Braga, Braga, Portugal

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Maria Lopes Pereira Department of Endocrinology, Hospital de Braga, Braga, Portugal

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Adrenal Tumors Study Group of the Portuguese Society of Endocrinology Department of Endocrinology, Centro Hospitalar do Porto, Porto, Portugal

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endocrinology residents from the 12 Portuguese centres. AD was diagnosed based on one of the following criteria: (1) a plasma adrenocorticotropic hormone (ACTH) concentration exceeding 66 pmol/L in combination with a low serum cortisol (<5 µg/dL); (2) an

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Nikolaj Rittig Department of Internal Medicine and Endocrinology (MEA) and Medical Research Laboratory, Aarhus University Hospital, Aarhus C, Denmark

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Mads Svart Department of Internal Medicine and Endocrinology (MEA) and Medical Research Laboratory, Aarhus University Hospital, Aarhus C, Denmark

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Niels Jessen Research Laboratory for Biochemical Pathology, Institute for Clinical Medicine, Aarhus University Hospital, Aarhus C, Denmark

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Niels Møller Department of Internal Medicine and Endocrinology (MEA) and Medical Research Laboratory, Aarhus University Hospital, Aarhus C, Denmark

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Holger J Møller Department of Clinical Biochemistry Aarhus University Hospital, Aarhus C, Denmark

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Henning Grønbæk Department of Hepatology and Gastroenterology, Aarhus University Hospital, Aarhus C, Denmark

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analysis Blood samples were stored at −20°C and analysed in the same assay after all participants had completed all trials. Serum concentrations of cortisol (ELISA, DRG Cortisol Enzyme Immunoassay Kit, Germany), glucagon (EMD Millipore’s Glucagon

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Thabiso R P Mofokeng Department of Medicine, University of the Free State, Bloemfontein, South Africa

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Salem A Beshyah Department of Medicine, Dubai Medical College, Duabi, United Arab Emirates
Department of Endocrinology, Mediclinic Airport Road Hospital, Abu Dhabi, United Arab Emirates

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Fazleh Mahomed Department of Medicine, University of the Free State, Bloemfontein, South Africa

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Kwazi C Z Ndlovu Department of Medicine, University of the Free State, Bloemfontein, South Africa

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Ian L Ross Division of Endocrinology, Department of Medicine, University of Cape Town, Cape Town, South Africa

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in addition to serum sodium and serum potassium only, clinical features and serum sodium and/or serum potassium in addition to relevant antibodies, or clinical features in addition to low serum cortisol with synthetic ACTH (tetracosactide) stimulation

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