Search for other papers by Nishchil Patel in
Google Scholar
PubMed
Search for other papers by Kagabo Hirwa in
Google Scholar
PubMed
Search for other papers by Gemma Gardner in
Google Scholar
PubMed
Search for other papers by Kirsten Pearce in
Google Scholar
PubMed
Search for other papers by Jinny Jeffery in
Google Scholar
PubMed
Search for other papers by Fizzah Iqbal in
Google Scholar
PubMed
Search for other papers by Daniel Flanagan in
Google Scholar
PubMed
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.
Search for other papers by Prachi Bansal in
Google Scholar
PubMed
Search for other papers by Anurag Lila in
Google Scholar
PubMed
Search for other papers by Manjunath Goroshi in
Google Scholar
PubMed
Search for other papers by Swati Jadhav in
Google Scholar
PubMed
Search for other papers by Nilesh Lomte in
Google Scholar
PubMed
Search for other papers by Kunal Thakkar in
Google Scholar
PubMed
Search for other papers by Atul Goel in
Google Scholar
PubMed
Search for other papers by Abhidha Shah in
Google Scholar
PubMed
Search for other papers by Shilpa Sankhe in
Google Scholar
PubMed
Search for other papers by Naina Goel in
Google Scholar
PubMed
Search for other papers by Neelam Jaguste in
Google Scholar
PubMed
Search for other papers by Tushar Bandgar in
Google Scholar
PubMed
Search for other papers by Nalini Shah in
Google Scholar
PubMed
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
Search for other papers by C E Higham in
Google Scholar
PubMed
The University of Liverpool, Brownlow Hill, Liverpool, UK
Search for other papers by A Olsson-Brown in
Google Scholar
PubMed
Search for other papers by P Carroll in
Google Scholar
PubMed
Search for other papers by T Cooksley in
Google Scholar
PubMed
Search for other papers by J Larkin in
Google Scholar
PubMed
Search for other papers by P Lorigan in
Google Scholar
PubMed
Search for other papers by D Morganstein in
Google Scholar
PubMed
Search for other papers by P J Trainer in
Google Scholar
PubMed
Search for other papers by the Society for Endocrinology Clinical Committee in
Google Scholar
PubMed
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
Search for other papers by Greta B Raglan in
Google Scholar
PubMed
Search for other papers by Louis A Schmidt in
Google Scholar
PubMed
Department of Neuroscience, Georgetown University, Washington, District of Columbia, USA
Search for other papers by Jay Schulkin in
Google Scholar
PubMed
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
Department of Neuroscience DNS, University of Padova, Padova, Italy
Search for other papers by Filippo Ceccato in
Google Scholar
PubMed
Nuclear Medicine Unit, Department of Medicine – DIMED, University-Hospital of Padova, Padova, Italy
Padova Neuroscience Center PNC, University of Padova, Padova, Italy
Search for other papers by Diego Cecchin in
Google Scholar
PubMed
Search for other papers by Michele Gregianin in
Google Scholar
PubMed
Search for other papers by Giacomo Ricci in
Google Scholar
PubMed
Department of Mathematics ‘Tullio Levi-Civita’ DM, University of Padova, Padova, Italy
Search for other papers by Cristina Campi in
Google Scholar
PubMed
Search for other papers by Filippo Crimì in
Google Scholar
PubMed
Search for other papers by Marta Bergamo in
Google Scholar
PubMed
Search for other papers by Annibale Versari in
Google Scholar
PubMed
Search for other papers by Carmelo Lacognata in
Google Scholar
PubMed
Search for other papers by Federico Rea in
Google Scholar
PubMed
Search for other papers by Mattia Barbot in
Google Scholar
PubMed
Search for other papers by Carla Scaroni in
Google Scholar
PubMed
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
Centre for Endocrinology, Diabetes and Metabolism, Birmingham Health Partners, Birmingham, UK
Search for other papers by Wiebke Arlt in
Google Scholar
PubMed
Search for other papers by the Society for Endocrinology Clinical Committee in
Google Scholar
PubMed
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
Search for other papers by Arno Téblick in
Google Scholar
PubMed
Search for other papers by Lies Langouche in
Google Scholar
PubMed
Search for other papers by Greet Van den Berghe in
Google Scholar
PubMed
, 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
Department of Neurosurgery, Rui-Jin Lu-Wan Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Search for other papers by Hong Jiang in
Google Scholar
PubMed
Search for other papers by WenJie Yang in
Google Scholar
PubMed
Department of Neurosurgery, Rui-Jin Lu-Wan Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China
Search for other papers by QingFang Sun in
Google Scholar
PubMed
College of Information Technology and Engineering, Chengdu University, Chengdu, China
College of Computer Science, Sichuan Normal University, Chengdu, Sichuan, China
Search for other papers by Chang Liu in
Google Scholar
PubMed
Search for other papers by LiuGuan Bian in
Google Scholar
PubMed
-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
Search for other papers by A Chinoy in
Google Scholar
PubMed
Search for other papers by M Skae in
Google Scholar
PubMed
Search for other papers by A Babiker in
Google Scholar
PubMed
Search for other papers by D Kendall in
Google Scholar
PubMed
Search for other papers by M Z Mughal in
Google Scholar
PubMed
Search for other papers by R Padidela in
Google Scholar
PubMed
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
Search for other papers by David J F Smith in
Google Scholar
PubMed
Search for other papers by Hemanth Prabhudev in
Google Scholar
PubMed
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
Search for other papers by Sirazum Choudhury in
Google Scholar
PubMed
Department of Investigative Medicine, Division of Diabetes, Endocrinology and Metabolism, Imperial College London, London, UK
Search for other papers by Karim Meeran in
Google Scholar
PubMed
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
