DOI: 10.36347/sjmcr.2024.v12i01.030

Pages: 115-118

Cushing's syndrome (CS), a rare endocrine disorder, is characterized by a diverse range of clinical manifestations due to prolonged exposure to excess glucocorticoids. CS can be divided into ACTH-dependent and ACTH-independent types, with varying degrees of clinical severity. Biochemical abnormalities, such as hypokalemia, are associated with CS, potentially resulting from the mineralocorticoid effects of cortisol. We present a unique case of Cushing's disease with a prominent and persistent feature of hypokalemia, even after a successful bilateral adrenalectomy. The patient's clinical presentation included sudden abdominal obesity, lumbago, polyuria, polydipsia, chronic constipation, muscle cramps, and profound weakness. Early diagnostic evaluation revealed severe hypokalemia requiring treatment. Despite bilateral adrenalectomy, hypokalemia persisted postoperatively, necessitating ongoing potassium supplementation. This case highlights the complex interplay of hormones in CS and the need for comprehensive clinical and biochemical assessments. Hypokalemia is prevalent in Cushing's syndrome (CS), typically resulting from renal potassium loss, influenced by cortisol's mineralocorticoid-like effects. Additionally, ACTH might inhibit 11β-HSD2, allowing cortisol to act as a mineralocorticoid. Persistent hypokalemia in our ACTH-dependent CS case, even after bilateral adrenalectomy, raises questions about the role of ACTH and 11β-HSD2. Further research is needed to clarify these mechanisms and their relationship with CS.