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Martin Wiegand MRC Biostatistics Unit, School of Clinical Medicine, University of Cambridge, Cambridge, UK

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David J Halsall Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Sarah L Cowan Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Kevin Taylor Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Robert J B Goudie MRC Biostatistics Unit, School of Clinical Medicine, University of Cambridge, Cambridge, UK

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Jacobus Preller Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK

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Mark Gurnell Cambridge University Hospitals NHS Foundation Trust, Cambridge, UK
Wellcome–MRC Institute of Metabolic Science, University of Cambridge and NIHR Cambridge Biomedical Research Centre, Addenbrooke’s Hospital, Cambridge, UK

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inhibition. The uninhibited AngII may then play a role in the pathogenesis of observed hypertension ( 6 ), inflammation, immunothrombosis and possible fibrosis in COVID-19. Whilst elevated serum cortisol has been identified as a marker of poor prognosis in

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Sweta Budyal Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Swati Sachin Jadhav Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Rajeev Kasaliwal Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Hiren Patt Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Shruti Khare Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Vyankatesh Shivane Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Anurag R Lila Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Tushar Bandgar Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Nalini S Shah Department of Endocrinology, Seth G S Medical College and KEM Hospital, Parel, Mumbai, Maharashtra 400012, India

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Introduction Subclinical Cushing's syndrome (SCS) is defined as autonomous cortisol secretion in patients without typical signs and symptoms of hypercortisolism, as in the classic Cushing's syndrome (CS) (1) . Screening for a rare disorder like SCS

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Ana Podbregar Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
University Rehabilitation Institute Republic of Slovenia, Ljubljana, Slovenia

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Tomaž Kocjan Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
Department of Endocrinology, Diabetes and Metabolic Disease, University Medical Center Ljubljana, Ljubljana, Slovenia

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Matej Rakuša Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
Department of Endocrinology, Diabetes and Metabolic Disease, University Medical Center Ljubljana, Ljubljana, Slovenia

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Peter Popović Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
Clinical Institute of Radiology, University Medical Center Ljubljana, Ljubljana, Slovenia

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Manca Garbajs Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
Clinical Institute of Radiology, University Medical Center Ljubljana, Ljubljana, Slovenia

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Katja Goricar Faculty of Medicine, Institute of Biochemistry, Pharmacogenetics Laboratory, University of Ljubljana, Ljubljana, Slovenia

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Andrej Janez Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
Department of Endocrinology, Diabetes and Metabolic Disease, University Medical Center Ljubljana, Ljubljana, Slovenia

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Mojca Jensterle Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia
Department of Endocrinology, Diabetes and Metabolic Disease, University Medical Center Ljubljana, Ljubljana, Slovenia

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-up ( 4 , 5 ), increases in NFAIs’ size and development of mild autonomous cortisol excess (MACE) over time have also been reported for this clinical entity ( 6 , 7 , 8 , 9 ). Currently, adequate long-term follow-up strategies of NFAIs after the

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Jan W Eriksson Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Reem A Emad Department of Pharmacy, Uppsala University, Uppsala, Sweden

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Martin H Lundqvist Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Niclas Abrahamsson Department of Medical Sciences, Uppsala University, Uppsala, Sweden

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Maria C Kjellsson Department of Pharmacy, Uppsala University, Uppsala, Sweden

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quantitative importance of other factors, such as inhibition by insulin and stimulation by amino acids, is disputed ( 8 , 9 ). Hypoglycemia also triggers the release of other counter-regulatory hormones such as catecholamines, cortisol, and growth hormone

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Paul-Martin Holterhus Department of Pediatrics I, Pediatric Endocrinology and Diabetology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian Albrechts University, CAU, Kiel, Germany

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Alexandra Kulle Department of Pediatrics I, Pediatric Endocrinology and Diabetology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian Albrechts University, CAU, Kiel, Germany

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Anne-Marie Till Department of Pediatrics, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Lübeck, Germany

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Caroline Stille Department of Pediatrics, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Lübeck, Germany

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Tabea Lamprecht Department of Pediatrics I, Pediatric Endocrinology and Diabetology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian Albrechts University, CAU, Kiel, Germany

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Simon Vieth Department of Pediatrics I, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Kiel and Christian-Albrechts-University, CAU, Kiel, Germany

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Melchior Lauten Department of Pediatrics, Pediatric Hematology and Oncology, University Hospital of Schleswig-Holstein, UKSH, Campus Lübeck, Germany

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glucocorticoid and mineralocorticoid biosynthesis ( 10 ). Both are typically at risk for adrenal crises in stress episodes. Interestingly, rare genetic subtypes of CAH like 11β hydroxylase deficiency (11βOHD) and 17 alpha/17–20 lyase deficiency block cortisol

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Katica Bajuk Studen Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia
Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia

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Simona Gaberšček Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia
Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia

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Edvard Pirnat Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia

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Nataša Bedernjak Bajuk Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia

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Andreja Vendramin Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia

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Vito Majcen Department of Nuclear Medicine, SB Celje, Celje, Slovenia

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Katja Zaletel Department of Nuclear Medicine, University Medical Centre Ljubljana, Ljubljana, Slovenia
Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia

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additional cortisol if needed ( 14 ). In accordance with this, a 30-day treatment protocol with a starting dose of 24 mg/day of methylprednisolone (MPSL) as the initial treatment for ST and tapered by 4 mg every 5 days is employed in our center. The

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Emmanuelle Motte UFR des Sciences de la Santé, Simone Veil, Université Versailles St-Quentin en Yvelines, Montigny le Bretonneux, France
Assistance Publique Hôpitaux de Paris (APHP), Department of Endocrinology and Diabetes for Children, Bicêtre Paris-Sud, Le Kremlin Bicêtre, France

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Anya Rothenbuhler Assistance Publique Hôpitaux de Paris (APHP), Department of Endocrinology and Diabetes for Children, Bicêtre Paris-Sud, Le Kremlin Bicêtre, France
APHP, Plateforme d’Expertise Maladies Rares Paris Sud, Bicêtre Paris Sud Hospital, Le Kremlin Bicêtre, France

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Stephan Gaillard Department of Neurosurgery, Foch Hospital, Suresnes, France

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Najiba Lahlou APHP, Department of Hormonal Biology, Cochin Hospital, Paris, France

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Cécile Teinturier Assistance Publique Hôpitaux de Paris (APHP), Department of Endocrinology and Diabetes for Children, Bicêtre Paris-Sud, Le Kremlin Bicêtre, France
APHP, Plateforme d’Expertise Maladies Rares Paris Sud, Bicêtre Paris Sud Hospital, Le Kremlin Bicêtre, France

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Régis Coutant Department of Pediatric Endocrinology, Angers University Hospital, Angers, France

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Agnès Linglart Assistance Publique Hôpitaux de Paris (APHP), Department of Endocrinology and Diabetes for Children, Bicêtre Paris-Sud, Le Kremlin Bicêtre, France
APHP, Plateforme d’Expertise Maladies Rares Paris Sud, Bicêtre Paris Sud Hospital, Le Kremlin Bicêtre, France

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Introduction Cushing’s disease (CD) is characterized by adrenocorticotropin (ACTH)-dependent cortisol excess originating from a pituitary adenoma and accounts for approximately 85% of cases of pediatric Cushing’s syndrome ( 1 , 2 , 3 , 4

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Alberto Giacinto Ambrogio Neuroendocrinology Research Laboratory, Istituto Auxologico Italiano IRCCS, Milan, Italy

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Massimiliano Andrioli Neuroendocrinology Research Laboratory, Istituto Auxologico Italiano IRCCS, Milan, Italy

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Martina De Martin Neuroendocrinology Research Laboratory, Istituto Auxologico Italiano IRCCS, Milan, Italy

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Francesco Cavagnini Neuroendocrinology Research Laboratory, Istituto Auxologico Italiano IRCCS, Milan, Italy

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Francesca Pecori Giraldi Neuroendocrinology Research Laboratory, Istituto Auxologico Italiano IRCCS, Milan, Italy
Department of Clinical Sciences and Community Health, University of Milan, Milan, Italy

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assess the pattern of ACTH/cortisol responses to desmopressin in the years following transsphenoidal surgery in patients with Cushing’s disease on long-term remission and to establish whether changes in the response to desmopressin in patients during

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Fidéline Bonnet-Serrano Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Hormonology Department, Cochin Hospital, Paris, France

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Maxime Barat Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Radiology Department, Cochin Hospital, Paris, France

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Anna Vaczlavik Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Anne Jouinot Inserm U1016-CNRS UMR8104, Paris, France

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Lucas Bouys Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Christelle Laguillier-Morizot Université Paris Cité, Paris, France
Hormonology Department, Cochin Hospital, Paris, France
INSERM, Physiopathologie et Pharmacotoxicologie Placentaire Humaine : Microbiote Pré & Post natal, Paris, France

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Corinne Zientek Hormonology Department, Cochin Hospital, Paris, France

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Catherine Simonneau Hormonology Department, Cochin Hospital, Paris, France

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Etienne Larger Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Diabetology Department, Cochin Hospital, Paris, France

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Laurence Guignat Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Lionel Groussin Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Guillaume Assié Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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Jean Guibourdenche Université Paris Cité, Paris, France
Hormonology Department, Cochin Hospital, Paris, France
INSERM, Physiopathologie et Pharmacotoxicologie Placentaire Humaine : Microbiote Pré & Post natal, Paris, France

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Ioannis Nicolis Université Paris Cité, Paris, France
UR 7537 BioSTM, Paris, France

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Marie-Claude Menet Institut de Chimie Physique, Université Paris-Saclay-CNRS, UMR8000, Orsay, France

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Jérôme Bertherat Université Paris Cité, Paris, France
Inserm U1016-CNRS UMR8104, Paris, France
Reference Center for Rare Adrenal Diseases, Endocrinology Department, Cochin Hospital, Paris, France

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series) but they can be responsible for autonomous cortisol secretion in about 12% of cases (1–29% among series) and for aldosterone secretion in 2.5% of cases (1.6–3.3% among series) ( 5 ). Primary bilateral macronodular adrenal hyperplasia (PBMAH) is

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Thomas Reinehr Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Alexandra Kulle Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University Hospital of Schleswig – Holstein, UKSH, Campus Kiel/Christian Albrechts University of Kiel, CAU, Kiel, Germany

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Juliane Rothermel Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Caroline Knop-Schmenn Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Nina Lass Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Christina Bosse Department of Pediatric Endocrinology, Diabetes, and Nutrition Medicine, Vestische Hospital for Children and Adolescents, University of Witten/Herdecke, Datteln, Germany

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Paul-Martin Holterhus Division of Pediatric Endocrinology and Diabetes, Department of Pediatrics, University Hospital of Schleswig – Holstein, UKSH, Campus Kiel/Christian Albrechts University of Kiel, CAU, Kiel, Germany

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, 21-deoxycorticosterone, deoxycorticosterone, corticosterone, 11-deoxycortisol, cortisol, cortisone, androstenedione, testosterone, dehydroepiandrostenedione sulfate (DHEA-S), estrone (E1), estradiol (E2), luteinizing hormone (LH), follicle

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