International Journal of Medical and Pharmaceutical Case Reports

Introduction: Iatrogenic Cushing syndrome is a common endocrine disorder caused by prolonged exposure to exogenous glucocorticoids. Long-term corticosteroid therapy can result in characteristic clinical features such as moon facies, hypertension, oedema, metabolic disturbances and suppression of the hypothalamic-pituitary-adrenal axis. Prednisolone is a widely prescribed glucocorticoid and a well-recognised cause of steroid-induced Cushing syndrome when used for prolonged periods without adequate monitoring.

Case Presentation: A 72-year-old female with a history of chronic knee joint pain and hypertension presented with facial puffiness, bilateral lower-limb swelling and retrosternal chest pain radiating to the back. Detailed history revealed prolonged unsupervised use of prednisolone for knee pain. Physical examination showed facial puffiness, pedal oedema and elevated blood pressure (180/110 mmHg). Laboratory investigations demonstrated mild anaemia, hypoalbuminaemia and a serum cortisol level of 8.22 µg/dL. Imaging studies revealed bilateral knee osteoarthritis, concentric left ventricular hypertrophy with Grade I diastolic dysfunction and hyperinflated lung fields.

Methodology: Clinical evaluation, laboratory investigations, imaging studies, medication-history assessment and causality assessment using the Naranjo Adverse Drug Reaction Probability Scale were performed. Prednisolone was discontinued and supportive therapy was initiated.

Discussion: The temporal relationship between prolonged prednisolone exposure and the development of characteristic clinical manifestations supported the diagnosis of steroid-induced Cushing syndrome. Despite a near-normal serum cortisol level, the patient's history and clinical findings were strongly suggestive of exogenous glucocorticoid excess. Improvement following withdrawal of prednisolone further reinforced the diagnosis. The Naranjo causality assessment score of 8 indicated a probable association between prednisolone therapy and the adverse event.

Conclusion: Early recognition of steroid-induced Cushing syndrome and prompt discontinuation of the offending corticosteroid are essential to prevent serious complications. Careful prescribing practices, regular monitoring and patient education regarding long-term steroid use are crucial for minimising the risk of glucocorticoid-related adverse effects and improving clinical outcomes. These predictors, however, require further work to validate their reliability in patients.