Adrenal Tumor Masquerading as Electrolyte Imbalance: A Case Report

Introduction: Hypokalemia is a recognized electrolyte abnormality seen in states of cortisol excess related to increased mineralocorticoid activity. Hypercortisolism, termed Cushing’s Syndrome, is commonly iatrogenic in the setting of glucocorticoid use. It is also encountered as an endogenous disorder due to either adrenocorticotropic hormone (ACTH)-dependent and ACTH-independent mechanisms. Adrenocortical carcinomas are uncommon, but are often hormonally active and patients present with signs of cortisol excess, including hypokalemia. We present such a case. Case Description: A 63-year-old female patient was admitted to the hospital for evaluation of hypokalemia. Recent routine lab work obtained by her primary care physician showed significant hypokalemia at 2.6 mmol/L. The patient reported fatigue and muscle cramps but denied rapid weight gain, sleep disturbances, or dermatologic changes. In the emergency department repeat labs confirmed hypokalemia at 2.0 mmol/L. Biochemical testing revealed an elevated serum cortisol level of 41.6 mcg/dL with suppressed ACTH <3 pg/mL, consistent with ACTH-independent hypercortisolism. An abdominal CT scan demonstrated a 4.4 cm left adrenal mass and multiple liver lesions suggestive of metastatic disease. Despite aggressive replacement and increasing doses of spironolactone and losartan for refractory hypokalemia, the endocrinology service recommended resection of the adrenal mass for definitive management. Discussion: The enzyme 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) is responsible for converting cortisol to its inactive form, cortisone, in the distal nephron thereby preventing cortisol from activating mineralocorticoid receptors. In hypercortisolism, 11β-HSD2 becomes saturated, allowing excess cortisol to bind and activate mineralocorticoid receptors. This leads to sodium retention, potassium excretion, and hydrogen ion loss, manifesting as hypertension, hypokalemia, and metabolic alkalosis—features similar to primary hyperaldosteronism. This case highlights the importance of considering cortisol-producing adrenal tumors in the differential diagnosis of refractory hypokalemia and underscores the pathophysiological overlap between hypercortisolism and hyperaldosteronism.