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Abstract: PO1115

Not Just Licorice: Abiraterone and Apparent Mineralocorticoid Excess

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

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

Authors

  • Beck, Natalie M., University of Colorado, Denver, Colorado, United States
  • Rizzolo, Katherine, University of Colorado, Denver, Colorado, United States
  • Ambruso, Sophia L., University of Colorado, Denver, Colorado, United States
Introduction

Abiraterone is a CYP17A1 inhibitor which blocks androgen synthesis and is used to treat castration-resistant prostate cancer. This drug also decreases cortisol synthesis, causing a compensatory increase in adrenocorticotropic hormone (ACTH) and accumulation of mineralocorticoids. The result is the syndrome of apparent mineralocorticoid excess (AME) which manifests clinically as hypokalemia, metabolic alkalosis and hypertension. Abiraterone is approved for use only with concurrent glucocorticoid replacement to prevent these effects. We present a case of refractory hypokalemia resulting from abiraterone use.

Case Description

A 74-year-old man with metastatic prostate cancer and head and neck cancer presented with urinary retention and acute kidney injury (AKI) as well as hypokalemia and metabolic alkalosis which were present a week prior. Home medications included abiraterone, cisplatin (given two weeks prior), prednisone 5 mg daily (recently decreased from 5 mg twice daily) and spironolactone. A urinary catheter was placed, the AKI improved rapidly and the patient remained with refractory hypokalemia. A urine potassium-to-creatinine ratio was high. Post-obstructive polyuria was considered as a reason for kaliuresis; however, hypokalemia and metabolic acidosis preceding this event made it unlikely to be the sole cause. Given abiraterone use, serum cortisol was checked and was low with no increase after giving cosyntropin. Serum aldosterone, renin and their ratio were normal. The patient was diagnosed with abiraterone-induced AME. Prednisone was increased to 5 mg twice daily and eplerenone was started in place of spironolactone. Two months later, the serum potassium was normal without supplementation.

Discussion

Abiraterone-induced AME is characterized by low serum cortisol but unlike adrenal insufficiency, presents with hypokalemia, metabolic alkalosis and hypertension. In this case, AME results from inhibition of the 17α-hydroxylase activity of the CYP17A1 enzyme, leading to decreased cortisol, increased ACTH, and accumulation of the potent mineralocorticoid dexoycorticosterone. Glucocorticoid supplementation (prednisone 5 mg twice daily recommended) is needed to suppress ACTH and prevent these effects. Eplerenone is an adjunct and is preferred over spironolactone in patients with castrate-resistant prostate cancer as spironolactone interacts with the androgen receptor.