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Abstract: TH-PO380

Refractory Hypokalemia in a Patient with Ectopic Adrenocorticotropic Hormone (ACTH) Secretion

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical


  • Cruz Peralta, Massiel Penelope, UPMC, Pittsburgh, Pennsylvania, United States
  • Abramovitz, Blaise William, UPMC, Pittsburgh, Pennsylvania, United States

Due to similarities in structure, aldosterone and cortisol bind to mineralocorticoid receptors with similar affinity. The enzyme 11ß-hydroxysteroid dehydrogenase (11ß-HSD) limits the effect of cortisol at this receptor by converting cortisol to cortisone which is inactive at this site. Deficiency in 11ß-HSD allows for unopposed cortisol stimulation at this receptor which mimics a state of mineralocorticoid excess. This condition manifests clinically with hypertension, hypokalemia, and metabolic alkalosis. We report a case of mineralocorticoid excess from ectopic production of ACTH leading to profound, refractory hypokalemia.

Case Description

A 56-year-old female with a history of COPD and large cell neuroendocrine carcinoma presented with one day of dyspnea, chills, and bilateral lower extremity edema. Lab work was remarkable for creatinine 1.4 mg/dL (baseline creatinine 0.7), tCO2 > 40 mmol/L, potassium of 2.2 mEq/L, and WBC 11.3 x 109/L with 87% neutrophils. CT angiography chest showed LLL subsegmental PE and multifocal pneumonia. The patient was admitted for management of pneumonia and started on IV fluids, broad-spectrum antibiotics, subcutaneous enoxaparin, and oral and IV potassium supplementation. She was noted to have worsening hypokalemia to 1.6 mEq/L despite aggressive repletion. A comprehensive chart review revealed nine months of intermittent episodes of moderate to severe hypokalemia and metabolic alkalosis starting one month after her neuroendocrine lung cancer diagnosis. A VBG showed pH 7.48, CO2 77 mmHg, and HCO3 56 mmol/L, suggestive of a primary metabolic alkalosis. 24-hour urine potassium was 68 mEq which confirmed inappropriately elevated urine potassium losses in the setting of severe hypokalemia. ACTH was elevated at 183 pg/mL (normal: 9-46), suggesting ectopic production of this hormone. 24-hour urine cortisol was 2086 mcg (normal: 4-50), confirming the suspicion of ectopic secretion of ACTH causing an apparent mineraloid corticoid excess picture. The patient was started on spironolactone and standing oral potassium replacement with subsequent improvement of her hypokalemia.


This case emphasizes the importance of thoroughly working up persistent hypokalemia. Ectopic ACTH production leading to mineralocorticoid excess in patients with malignancy is a rare occurrence. Without establishing a diagnosis, appropriate management cannot be sought.