SUN-258 - Refractory Hypokalemia in Patient with Prostate Cancer on Abiraterone and Prednisone

Abiraterone is an anti-androgen therapy used in advanced prostate cancer. It inhibits androgen and cortisol synthesis by irreversibly blocking CYP17A1 enzyme. The feedback loop stimulates adrenocorticotropic hormone (ACTH), which increases the production of mineralocorticoid. Glucocorticoid is co-administered with abiraterone to suppress ACTH and prevent the downstream effect. Insufficient suppression of ACTH can result in mineralocorticoid excess syndrome (MES), characterized by electrolyte imbalances, hypertension, and volume expansion.

We present a 79-year-old male who was hospitalized after a fall and found to have refractory hypokalemia (Potassium: 1.9 mmol/L) and hypertension. His medical history was significant for castration sensitive prostate cancer which was status post prostatectomy, salvage radiation, and androgen deprivation therapy, followed by abiraterone, prednisone 5 mg daily and potassium chloride 40 mEq daily which started nine months before his admission. Despite the intervention, potassium remained low at 2.7 mmol/L. To more effectively suppress ACTH, 0.5 mg dexamethasone was added nightly. Potassium levels and the blood pressure gradually improved over the next few days. Dexamethasone was discontinued before discharge, and the patient was sent home with a steroid taper and close outpatient follow-up. His oncologist discontinued abiraterone and pursued alternative treatments.

Studies show that 20% of patients on abiraterone develop hypokalemia varied by steroid dosing. However, higher doses of steroids, except dexamethasone, can activate androgen receptors in prostate cancer limiting their use. Dexamethasone use is limited due to its strong potency and complication of hypercortisolism. Mineralocorticoid antagonists, such as finerenone or eplerenone, are considered alternatives to steroids for hypokalemia, though these can be cost-prohibitive. Spironolactone should be avoided due to concern of its action as a partial androgen receptor agonist which interferes with the cancer treatment. Amiloride, in combination with hydrochlorothiazide, offers another alternative, though its efficacy is unclear. This case highlights the need for early recognition and management of MES, which can cause significant complications of prostate cancer treatment. Further research is needed to better understand acute treatment strategies, assess the efficacy of alternative therapies, and explore potential novel treatment options.

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