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Nishchil Patel N Patel, Endocrinology and Diabetes, University Hospitals Plymouth NHS Trust, Plymouth, PL6 8DH, United Kingdom of Great Britain and Northern Ireland

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Kagabo Hirwa K Hirwa, Department of Endocrinology, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Gemma Gardner G Gardner, Endocrinology and Diabetes, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Kirsten Pearce K Pearce, Department of Neuroradiology, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Jinny Jeffery J Jeffery, Department of Biochemistry, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Fizzah Iqbal F Iqbal, Morriston Hospital, Swansea, United Kingdom of Great Britain and Northern Ireland

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Daniel Flanagan D Flanagan, Department of Endocrinology, University Hospitals Plymouth NHS Trust, Plymouth, United Kingdom of Great Britain and Northern Ireland

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Aim: To define functional and anatomical pituitary disease following ICI therapy and describe any change in pituitary function with time.

Methods: Retrospective observational audit of patients on ICI therapy in our centre between 2013 and 2023. We reviewed all patients on ICI therapy under the oncology department at University Hospital Plymouth, and identified individuals referred to endocrinology with suspected adrenal insufficiency. Patients were established on adrenal steroid replacement and subsequently underwent formal pituitary testing. Pituitary disease was evidenced by low ACTH, other pituitary dysfunction and/or abnormalities on pituitary imaging.

Results: 954 patients received ICI therapy during the study period, and 37 developed HPA axis dysfunction. Median interval of onset of symptoms was 4 months. There was no recovery in cortisol or ACTH for any individual on repeated testing. Other permanent anterior pituitary hormone defects were unusual. Hypophysitis associated with immunotherapy appears to specifically target corticotrophs with no evidence of recovery. There was a specific abnormality seen in MRI scans of 7 of 27 patients who had scans, appearing to be a particular feature of immune mediated hypophysitis. These were confined to the anterior aspect of the pituitary as striations and were not visible on any scans performed more than three months after disease onset.

Conclusion: These data show that immune related (IR) hypophysitis is a common complication of immune checkpoint inhibitor therapy. This may result in an imaging abnormality within the areas of the pituitary richest in corticotrophs. The endocrine consequence of this is a permanent defect in ACTH and therefore cortisol production.

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Prachi Bansal Department of Endocrinology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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

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Manjunath Goroshi Department of Endocrinology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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

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Nilesh Lomte Department of Endocrinology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Kunal Thakkar Department of Endocrinology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Atul Goel Department of Neurosurgery, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Abhidha Shah Department of Neurosurgery, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Shilpa Sankhe Department of Radiology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Naina Goel Department of Pathology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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Neelam Jaguste Department of Endocrinology, Seth G.S. Medical College and KEM Hospital, Mumbai, Maharashtra, India

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

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

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Introduction Cushing’s disease (CD) is a state of cortisol excess, caused by an ACTH-secreting pituitary adenoma. Although a rare disease with an annual incidence of 1.5 patients/million ( 1 ), it is associated with significant morbidity and

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C E Higham Department of Endocrinology, Christie Hospital NHS Foundation Trust, Manchester, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK

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A Olsson-Brown The Clatterbridge Cancer Centre, Bebbington, Wirral, UK
The University of Liverpool, Brownlow Hill, Liverpool, UK

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P Carroll Department of Endocrinology, Guy’s & St. Thomas’ NHS Foundation Trust, London, UK

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T Cooksley Department of Acute Medicine, UHSM and Christie Hospital NHS Foundation Trust, Manchester, UK

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J Larkin Skin Unit, Royal Marsden Hospital, London, UK

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P Lorigan Department of Medical Oncology, Christie Hospital NHS Foundation Trust, Manchester, UK

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D Morganstein Department of Endocrinology, Chelsea and Westminster Hospital, London, UK

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P J Trainer Department of Endocrinology, Christie Hospital NHS Foundation Trust, Manchester, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK

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the Society for Endocrinology Clinical Committee The Society for Endocrinology, Starling House, 1600 Bristol Parkway North, Bristol, UK

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screening. CTCAE grade 1–2. Other important considerations; hypophysitis and maintenance glucocorticoid therapy. Management of a life-threateningly unwell patient (CTCAE grade 3–4) Cortisol Features of acute cortisol

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Greta B Raglan Department of Psychology, American University, Washington, District of Columbia, USA

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Louis A Schmidt Department of Psychology, Neuroscience & Behavior, McMaster University, Hamilton, Ontario, Canada

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Jay Schulkin Department of Research, American College of Obstetricians and Gynecologists, Washington, District of Columbia, USA
Department of Neuroscience, Georgetown University, Washington, District of Columbia, USA

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glucocorticoid levels and high anxiety. Despite this, individuals with PTSD also have higher levels of CRH in the cerebral spinal fluid ( 27 ) and appear to have similar cortisol reactivity to individuals without the disorder ( 28 ). Based on these findings, it

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Filippo Ceccato Endocrinology Unit, Department of Medicine DIMED, University-Hospital of Padova, Padova, Italy
Department of Neuroscience DNS, University of Padova, Padova, Italy

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Diego Cecchin Department of Neuroscience DNS, University of Padova, Padova, Italy
Nuclear Medicine Unit, Department of Medicine – DIMED, University-Hospital of Padova, Padova, Italy
Padova Neuroscience Center PNC, University of Padova, Padova, Italy

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Michele Gregianin Nuclear Medicine Unit, Castelfranco Veneto, Italy

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Giacomo Ricci Department of Neuroscience DNS, University of Padova, Padova, Italy

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Cristina Campi Padova Neuroscience Center PNC, University of Padova, Padova, Italy
Department of Mathematics ‘Tullio Levi-Civita’ DM, University of Padova, Padova, Italy

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Filippo Crimì Radiology Unit, Department of Medicine DIMED, University-Hospital of Padova, Padova, Italy

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Marta Bergamo Endocrinology Unit, Department of Medicine DIMED, University-Hospital of Padova, Padova, Italy

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Annibale Versari Nuclear Medicine Unit, Reggio Emilia, Italy

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Carmelo Lacognata Radiology Department, University-Hospital of Padova, Padova, Italy

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Federico Rea Thoracic Surgery Unit, Department of Cardiac, Thoracic and Vascular Sciences, University Hospital of Padova, Padova, Italy

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Mattia Barbot Endocrinology Unit, Department of Medicine DIMED, University-Hospital of Padova, Padova, Italy

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Carla Scaroni Endocrinology Unit, Department of Medicine DIMED, University-Hospital of Padova, Padova, Italy

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Introduction Cushing’s syndrome (CS), characterized by excessive endogenous cortisol secretion, is in most cases ACTH-dependent. Corticotropin (ACTH) secretion arises from a pituitary adenoma (Cushing’s disease) or, less frequently, from a non

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Wiebke Arlt Institute of Metabolism and Systems Research, University of Birmingham, Birmingham, UK
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK

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the Society for Endocrinology Clinical Committee The Society for Endocrinology, 22 Apex Court, Woodlands, Bradley Stoke, Bristol, UK

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Introduction Acute adrenal insufficiency , also termed adrenal crisis , is a life-threatening endocrine emergency brought about by a lack of production of the adrenal hormone cortisol, the major glucocorticoid. Identifying patients at risk

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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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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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, the rate-limiting step in adrenal steroidogenesis, is also upregulated by ACTH-induced MC2R activation ( 43 ). Likewise, the final enzyme for cortisol synthesis, 11-β-hydroxylase, which converts 11-deoxycortisol into cortisol is upregulated upon ACTH

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Hong Jiang Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Department of Neurosurgery, Rui-Jin Lu-Wan Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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WenJie Yang Department of Radiology, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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QingFang Sun Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Department of Neurosurgery, Rui-Jin Lu-Wan Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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Chang Liu The Clinical Hospital of Chengdu Brain Science Institute, MOE Key Lab for Neuroinformation, Center for Information in Medicine, University of Electronic Science and Technology of China, Chengdu, China
College of Information Technology and Engineering, Chengdu University, Chengdu, China
College of Computer Science, Sichuan Normal University, Chengdu, Sichuan, China

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LiuGuan Bian Department of Neurosurgery, Rui-Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

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-h urinary free cortisol (UFC) level, bilateral petrosal sinus sampling, absence of a blunted circadian rhythm of cortisol secretion, and other clinical features ( 18 ). CD remission was confirmed in all remitted CD patients by normal UFC after

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A Chinoy Royal Manchester Children’s Hospital, Manchester, UK

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M Skae Royal Manchester Children’s Hospital, Manchester, UK

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A Babiker King Abdullah Specialized Children’s Hospital, Riyadh, Saudi Arabia

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D Kendall Royal Preston Hospital, Preston, UK

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M Z Mughal Royal Manchester Children’s Hospital, Manchester, UK

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R Padidela Royal Manchester Children’s Hospital, Manchester, UK

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intake. However, our cases were tolerating feeds during their illness (barring case 1 during early phase of illness). We postulate that this phenomenon may involve cortisol-driven effects on 1,25(OH) 2 -vitamin D. It is recognised that the stress of

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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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which treatment with supraphysiological doses of exogenous steroid is required. The aim of glucocorticoid replacement therapy in adrenal failure is to reverse the deficiency using only physiological doses of steroids. Reproducing the diurnal cortisol

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