IntroductionEctopic ACTH secretion accounts for approximately 10–20% of cases of ACTH-dependent Cushing’s syndrome and is most commonly associated with pulmonary neuroendocrine tumours and small-cell lung carcinoma (1). Gastrointestinal sources are rare and frequently under-recognised, particularly in cases without classical phenotypic features of hypercortisolism (1,3).Mortality in untreated ectopic ACTH syndrome is largely driven by severe metabolic complications, thromboembolism, and infectious sequelae secondary to profound hypercortisolism (2). Early recognition is therefore essential.In acute and general medical settings, electrolyte disturbances in oncology patients are commonly attributed to gastrointestinal losses, chemotherapy-related effects, or poor oral intake. Failure to recognise hormonally mediated causes may result in repeated admissions, delayed diagnosis, and increased morbidity. This case illustrates how ectopic ACTH secretion may present primarily as severe metabolic instability rather than overt Cushingoid phenotype.
