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  • glucocorticoid replacement x
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David J F Smith 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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Sirazum Choudhury Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK
Department of Clinical Biochemistry, Imperial College Healthcare NHS Trust, London, UK
Department of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK

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

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mineralocorticoid production in primary adrenal failure. The mainstay of treatment is glucocorticoid replacement, with either hydrocortisone or prednisolone ( 2 ). Both work by binding to the glucocorticoid receptor (GR) for which prednisolone has the greater

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-17-0257
Volume/Issue:
Volume 6: Issue 8
Open access
Sirazum Choudhury Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, Commonwealth Building, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Tricia Tan Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, Commonwealth Building, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Katharine Lazarus Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, Commonwealth Building, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Karim Meeran Endocrinology and Investigative Medicine, Department of Metabolism, Digestion and Reproduction, Imperial College London, Commonwealth Building, London, UK
Department of Endocrinology, Imperial College Healthcare NHS Trust, London, UK

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Introduction Between 1928 and 1938, patients with Addison’s disease had a 100% 5-year mortality ( 1 ). With the availability of glucocorticoid replacement therapy, initially with animal adrenocortical extract and later synthetic 11

Article Type:
Review Article
DOI:
https://doi.org/10.1530/EC-20-0473
Volume/Issue:
Volume 10: Issue 2
Open access
Johan G Beun AdrenalNET, The Netherlands

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Pia Burman Department of Endocrinology, Skåne University Hospital, Lund University, Sweden

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Olle Kämpe Department of Medicine (Solna), Centre for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden
Department of Endocrinology, Diabetes and Metabolism, Karolinska University Hospital, Stockholm, Sweden

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Eystein S Husebye Department of Clinical Science, University of Bergen, Bergen, Norway
Department of Medicine, Haukeland University Hospital, Bergen, Norway

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Stephanie Hahner Division of Endocrinology and Diabetes, University Hospital of Wuerzburg, Germany

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Jette Kristensen Addison Foreningen i Danmark, Denmark

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Alida Noordzij AdrenalNET, The Netherlands

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Per Dahlqvist Department of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden

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hormone. Once diagnosed, chronic, daily replacement with glucocorticoids is essential. An adequate hormone replacement dose is considered to be a total of 15–25 mg hydrocortisone (or cortisone acetate 20–35 mg per day) in adults in two to three daily doses

Article Type:
Review Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0345
Volume/Issue:
Volume 12: Issue 1
Open access
Salem A Beshyah Department of Medicine, Dubai Medical College, Dubai, United Arab Emirates
Diabetes and Endocrine Clinic, Mediclinic Airport Road Hospital, Abu Dhabi, United Arab Emirates

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Khawla F Ali Department of Medicine, Royal College of Surgeons in Ireland Medical University of Bahrain, Adliya, Bahrain

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Hussein F Saadi Department of Endocrinology, Medical Subspecialties Institute, Cleveland Clinic Abu Dhabi, Abu Dhabi, United Arab Emirates

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preparation do you, most commonly, use for replacement therapy? (Hydrocortisone, Cortisone acetate, Prednisone/Prednisolone, Long-acting prednisolone, Dexamethasone).  4. How do you usually divide the daily dose of glucocorticoids used for replacement

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-20-0314
Volume/Issue:
Volume 9: Issue 8
Open access
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

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0143
Volume/Issue:
Volume 11: Issue 7
Open access
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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is important for clinicians to be aware of the heterogeneity in endogenous glucocorticoid secretion to prevent over-replacement with potential deleterious effect on bone density and metabolic profile. Case 2 in our series is the third documented case

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-22-0305
Volume/Issue:
Volume 12: Issue 1
Open access
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

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-23-0059
Volume/Issue:
Volume 12: Issue 9
Open access
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

Article Type:
Research Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-23-0097
Volume/Issue:
Volume 12: Issue 8
Open access
Deirdre Green Academic Department of Endocrinology, Beaumont Hospital and the Royal College of Surgeons in Ireland, Dublin

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Rosemary Dineen Academic Department of Endocrinology, Beaumont Hospital and the Royal College of Surgeons in Ireland, Dublin

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Michael W O’Reilly Academic Department of Endocrinology, Beaumont Hospital and the Royal College of Surgeons in Ireland, Dublin

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Mark Sherlock Academic Department of Endocrinology, Beaumont Hospital and the Royal College of Surgeons in Ireland, Dublin

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). Undiagnosed AI, therefore, leads to significant morbidity and mortality ( 8 , 9 ). All patients with AI require glucocorticoid (GC) replacement; however, in contrast to PAI, patients with ACTH deficiency (SAI and TAI) do not require mineralocorticoid

Article Type:
Review Article
Collections:
Adrenal
DOI:
https://doi.org/10.1530/EC-23-0088
Volume/Issue:
Volume 13: Issue 2
Open access
Kathrin R Frey Department of Medicine I, Endocrine and Diabetes Unit, University Hospital, University of Würzburg, Würzburg, Germany

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Tina Kienitz Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

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Julia Schulz Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

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Manfred Ventz Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

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Kathrin Zopf Charité – Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany

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Marcus Quinkler Endocrinology in Charlottenburg, Berlin, Germany

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Introduction In states of adrenal insufficiency (AI), such as primary adrenal insufficiency (PAI) and congenital adrenal hyperplasia (CAH), glucocorticoids (GCs) are given in low doses as hormone replacement therapy. However, the daily intake

Article Type:
Research Article
DOI:
https://doi.org/10.1530/EC-18-0160
Volume/Issue:
Volume 7: Issue 6
Open access