Critical illness-related corticosteroid insufficiency (CIRCI) presents as refractory hemodynamic shock in critically ill patients. Research on CIRCI and its treatment in burn patients is limited. We sought to review the use of corticosteroids in a burn population during their first week of hospitalization. The burn registry and the electronic medical records were queried for burn patients admitted between January 2015 and December 2025. The following variables were abstracted: demographics, burn history, hospital course, and treatments. Outcome variables included length of stay (LOS), infections, graft loss, pharmacological treatment, and mortality. The two groups were compared with Student's T-test and Chi Square where appropriate. A multivariant analysis was performed to determine independent predictors of CIRCI, infection and mortality. Significance was determined at p<0.05 level. The study group consisted of 87 patients in hemodynamic shock receiving vasopressors, with 47 also receiving corticosteroids. The corticosteroid group had larger burns (37.6 v 25.1%), more resuscitation (15.9 v 8.1 L), more vasopressor days (6.23 v 3.7 d), more ventilator days (19.72 v 7.83 d), more infections (66% v 34%) and longer LOS (51.53 v 26.05 d), all p<0.05. On multivariant analysis, variables independently related to the diagnosis of CIRCI were age and resuscitation fluids; to infection were corticosteroid use; and to mortality were age. Overall, over 50% of patients in hypotensive shock during their first week of treatment were diagnosed and treated with corticosteroids for suspected CIRCI. More study is needed to determine the appropriate role of corticosteroid use in early burn treatment.

Immune checkpoint inhibitor-associated hypophysitis is an uncommon but clinically important endocrine immune-related adverse event. We report a 70-year-old man with a history of non-small cell lung cancer previously treated with approximately two years of pembrolizumab, with his last dose administered approximately 28 months before presentation. He developed progressive fatigue, anorexia, hypotension, functional decline, and confusion and was subsequently hospitalized with multifocal pneumonia and septic shock. Although the infection and hemodynamic instability improved, encephalopathy, weakness, poor oral intake, and dysphagia persisted. Brain magnetic resonance imaging demonstrated new pituitary enlargement compared with imaging obtained approximately three months earlier. Dedicated pituitary imaging showed enlargement measuring approximately 1.5 × 2.0 cm without definite differential enhancement to suggest a pituitary adenoma. Endocrine testing demonstrated a cortisol level of 3.3 µg/dL with an inappropriately low adrenocorticotropic hormone level of 6.5 pg/mL, free thyroxine of 0.36 ng/dL with thyroid-stimulating hormone of 2.0 µIU/mL, suppressed gonadotropins, and testosterone <10 ng/dL, supporting central adrenal insufficiency and central hypothyroidism with marked gonadal-axis suppression. Cerebrospinal fluid cytology and paraneoplastic studies were unrevealing. The patient was treated with hydrocortisone before thyroid hormone replacement and subsequently showed progressive improvement in mental status, oral intake, and participation in rehabilitation. This case highlights that pituitary immune-related adverse events may be recognized long after pembrolizumab discontinuation and emphasizes the importance of considering prior immune checkpoint inhibitor exposure in patients with unexplained endocrine and constitutional decline.

Potent topical corticosteroids can be absorbed systemically and cause both iatrogenic Cushing syndrome and suppression of endogenous cortisol production. Most paediatric reports involve infants, so clinically important toxicity in adolescents may be overlooked. A 15-year-old girl used clobetasol propionate 0.05% ointment for six months, with a reported cumulative exposure of 250 g and no documented interim clinical review. She developed Cushingoid facial changes, extensive lower-limb striae, fatigue, impaired concentration, insomnia, and low mood. Morning cortisol was <30 nmol/L and ACTH was <5 ng/L. An initial short Synacthen test showed cortisol concentrations of <30 nmol/L at baseline and 30 minutes and 38 nmol/L at 60 minutes, confirming severely impaired adrenal reserve. Clobetasol was discontinued. The patient was started on physiological hydrocortisone replacement, educated on sick-day rules, and supplied with emergency intramuscular hydrocortisone. Serial Synacthen testing showed partial recovery at 2.5 months and adequate adrenal reserve by seven months, allowing hydrocortisone to be discontinued. Her mood subsequently improved, while the striae faded gradually. This case demonstrates a compelling association between prolonged exposure to a very potent topical corticosteroid, clobetasol, and the development of simultaneous Cushingoid features and glucocorticoid-induced adrenal insufficiency in an adolescent. Careful diagnostic review, patient counselling, planned clinical monitoring, and recognition of adrenal suppression are important medication-safety measures when potent or very potent topical corticosteroids are prescribed.

Primary bilateral macronodular adrenal hyperplasia (PBMAH) is a rare cause of Cushing syndrome (CS), characterized by bilateral adrenal nodules larger than 1 cm. Cortisol hypersecretion in PBMAH is driven by intra-adrenal rather than pituitary adrenocorticotropic hormone (ACTH), with its pathogenesis mediated by aberrant hormone receptor expression in the adrenal cortex. This article reports a case of a 60-year-old woman with PBMAH in whom a marked reduction in bilateral adrenal masses was observed following treatment with osilodrostat. The patient presented with typical Cushingoid features, accompanied by hypertension, diabetes mellitus, osteoporosis, and severe restrictive lung disease. Genetic testing identified a pathogenic mutation in the ARMC5 gene, confirming the diagnosis. Because she was intolerant of surgical treatment, left adrenal artery embolization (AAE) was performed but failed to control hypercortisolism. Osilodrostat therapy was subsequently initiated-this potent 11β-hydroxylase inhibitor was recently approved in China for the treatment of Cushing syndrome. Notably, after 23 weeks of treatment, the patient's 24-hour urinary free cortisol (24 hours-UFC, CLIA) level returned to normal. Treatment was then discontinued, and during 11 months of follow-up the patient's 24 hours-UFC remained within the normal range. Moreover, imaging performed during the period of osilodrostat therapy demonstrated significant shrinkage of both adrenal glands. To our knowledge, this is the first reported case of bilateral adrenal mass reduction observed in temporal association with osilodrostat treatment in a PBMAH patient. However, prior AAE confounds the attribution of tumor shrinkage to osilodrostat alone. These findings highlight an observed association between the drug and mass reduction, warranting further investigation to clarify its potential role beyond symptomatic control.