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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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Introduction High-dose glucocorticoids are indispensable in the treatment of childhood acute lymphoblastic leukemia (ALL) ( 1 ). Two different highly potent synthetic glucocorticoids are used in the current standard protocols, namely

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Clara Lundetoft Clausen Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark

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Trine Holm Johannsen Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Niels Erik Skakkebæk Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Hanne Frederiksen Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark

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Anders Juul Department of Growth and Reproduction, Copenhagen University Hospital - Rigshospitalet, Copenhagen, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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Thomas Benfield Center of Research & Disruption of Infectious Diseases, Department of Infectious Diseases, Copenhagen University Hospital - Amager and Hvidovre, Hvidovre, Denmark
Department of Clinical Medicine, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark

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critical illness including septic shock, community-acquired pneumonia (CAP), and acute respiratory distress syndrome ( 7 , 8 ). In the management of hypoxic COVID-19, dexamethasone, a synthetic glucocorticoid, plays a crucial role in reducing mortality ( 9

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Huifei Sophia Zheng Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Jeffrey G Daniel Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Julia M Salamat Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Laci Mackay Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Chad D Foradori Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Robert J Kemppainen Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Satyanarayana R Pondugula Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Ya-Xiong Tao Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Chen-Che Jeff Huang Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, Alabama

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Introduction Glucocorticoids (GCs) are primary stress hormones and critical regulators of several physiological mechanisms. GCs commonly elicit their function through glucocorticoid receptor (GR)-mediated genomic effects. However, these

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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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Introduction Patients with adrenal insufficiency (AI) have premature morbidity and mortality ( 1 ). Mildly elevated levels of glucocorticoids or non-circadian timing of therapy may contribute towards cardiovascular disease and increased

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Riccardo Pofi Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism and NIHR Oxford Biomedical Research Centre, Churchill Hospital, University of Oxford, Oxford, UK

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Ilaria Bonaventura Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena, Rome, Italy

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Joanne Duffy Department of Clinical Chemistry and Immunology, Heartlands Hospital, Birmingham, UK

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Zoe Maunsell Department of Clinical Biochemistry, Oxford University Hospitals NHS Foundation Trust, Oxford, UK

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Brian Shine Department of Clinical Biochemistry, Oxford University Hospitals NHS Foundation Trust, Oxford, UK

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Andrea M Isidori Department of Experimental Medicine, Sapienza University of Rome, Viale Regina Elena, Rome, Italy

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Jeremy W Tomlinson Department of Endocrinology, Oxford Centre for Diabetes, Endocrinology and Metabolism and NIHR Oxford Biomedical Research Centre, Churchill Hospital, University of Oxford, Oxford, UK

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Introduction Primary adrenal insufficiency (PAI) is a rare disease consisting of the inability of the adrenal cortex to produce adequate levels of glucocorticoids (GCs), with or without concomitant inadequate production of mineralocorticoids

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Hanna F Nowotny Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Jillian Bryce Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Salma R Ali Office for Rare Conditions, University of Glasgow, Glasgow, UK

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Roberta Giordano Department of Clinical and Biological Sciences, University of Turin, Turin, Italy
Division of Endocrinology, Diabetes and Metabolism, Department of Medical Sciences, University of Turin, Turin, Italy

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Federico Baronio Pediatric Unit, Department Hospital of Woman and Child, Endo-ERN Centre IT11, IRCSS AOU S.Orsola-Malpighi University Hospital, Bologna, Italy

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Irina Chifu Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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Lea Tschaidse Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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Martine Cools Department of Paediatric Endocrinology, Ghent University Hospital, University of Ghent, Ghent, Belgium

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Erica LT van den Akker Department of Pediatrics, Division of Pediatric Endocrinology, Erasmus MC - Sophia Children’s Hospital, Erasmus University Medical Center, Rotterdam, The Netherlands

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Henrik Falhammar Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden
Department of Endocrinology, Karolinska University Hospital, Stockholm, Sweden

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Natasha M Appelman-Dijkstra Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Luca Persani Department of Endocrine and Metabolic Diseases, Istituto Auxologico Italiano IRCCS, Milan, Italy
Department of Medical Biotechnology and Translational Medicine, University of Milan, Milan Italy

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Guglielmo Beccuti Department of Clinical and Biological Sciences, University of Turin, Turin, Italy

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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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Simona Grozinsky-Glasberg Neuroendocrine Tumor Unit, ENETS Center of Excellence, Department of Endocrinology and Metabolism, Hadassah Medical Organisation and Faculty of Medicine, the Hebrew University, Jerusalem, Israel

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Alberto M Pereira Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands

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Eystein S Husebye Department of Clinical Science and KG Jebsen Center for Autoimmune Disorders, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway
Department of Medicine, Karolinska Institutet, Stockholm, Sweden

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Stefanie Hahner Division of Endocrinology and Diabetology, Department of Internal Medicine I, University Hospital of Wuerzburg, University of Wuerzburg, Wuerzburg, Germany

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S Faisal Ahmed Office for Rare Conditions, University of Glasgow, Glasgow, UK
Department of Medicine, Division of Endocrinology, Leiden University Medical Center, Leiden, The Netherlands
Developmental Endocrinology Research Group, University of Glasgow, Glasgow, United Kingdom

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Nicole Reisch Medizinische Klinik IV, Department of Endocrinology, Klinikum der Universität München, Munich, Germany

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AI and long-term glucocorticoid substitution therapy or glucocorticoid excess in Cushing’s syndrome (CS), are regularly prone to infections, especially those of the upper airways and gastrointestinal tract, due to impaired immune cell function ( 17

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Margret J Einarsdottir Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Penelope Trimpou Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Gudmundur Johannsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden

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Oskar Ragnarsson Department of Internal Medicine and Clinical Nutrition, Institute of Medicine at Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden
Department of Endocrinology, Sahlgrenska University Hospital, Gothenburg, Sweden
Wallenberg Center for Molecular and Translational Medicine, University of Gothenburg, Gothenburg, Sweden

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Introduction Oral glucocorticoid (GC) treatment can lead to adrenal insufficiency by suppressing the hypothalamic–pituitary–adrenal axis. This can result in life-threatening adrenal crisis if the patient does not receive an increased GC dose

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Arno Téblick Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Ilse Vanhorebeek Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Inge Derese Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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An Jacobs Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Renata Haghedooren Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Sofie Maebe Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Gerdien A Zeilmaker-Roest Department of Neonatal & Pediatric Intensive Care, Division of Pediatric Intensive Care, Erasmus MC – Sophia Children’s Hospital, Rotterdam, the Netherlands

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Enno D Wildschut Department of Neonatal & Pediatric Intensive Care, Division of Pediatric Intensive Care, Erasmus MC – Sophia Children’s Hospital, Rotterdam, the Netherlands

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Lies Langouche Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Greet Van den Berghe Clinical Division and Laboratory of Intensive Care Medicine, Department of Cellular and Molecular Medicine, KU Leuven, Leuven, Belgium

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Introduction Recently, we have found that during critical illness, the well-known constellation of ‘low plasma ACTH in the face of increased systemic glucocorticoid availability’ coincides with a substantial increase in plasma concentrations

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Ditte Sofie Dahl Sørensen Department of Endocrinology and Metabolism, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Jesper Krogh Department of Endocrinology and Metabolism, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Åse Krogh Rasmussen Department of Endocrinology and Metabolism, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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Mikkel Andreassen Department of Endocrinology and Metabolism, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark

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profiles in adult patients with 21-hydroxylase deficiency have shown a substantial circadian rhythm highly influenced by glucocorticoid replacement ( 6 ). Most recent clinical guideline from the US Endocrine Society suggests levels of androstenedione and 17

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Sophie Howarth Clinical and Translational Research Institute, Newcastle University, Newcastle upon Tyne, UK
Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK

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Luca Giovanelli Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK

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Catherine Napier Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK

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Simon H Pearce Clinical and Translational Research Institute, Newcastle University, Newcastle upon Tyne, UK
Department of Endocrinology, The Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK

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insufficient to meet the body’s needs. Overt mineralocorticoid deficiency causes the characteristic presentation of salt craving, postural hypotension, hyponatraemia and hyperkalaemia. Glucocorticoid deficiency causes loss of appetite, early satiety, weight

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