Case Presentation: A 75-year-old man presented to the emergency department (ED) at the request of Oncology after outpatient labs showed hypokalemia. Past medical history was notable for metastatic castrate-sensitive prostate cancer. He was on androgen-deprivation therapy (ADT) and had previously been prescribed abiraterone and prednisone, however both were recently stopped after an admission at another hospital one month prior for sustained ventricular tachycardia. The episode of sustained ventricular tachycardia was attributed to hypokalemia. On the day of presentation to our hospital, he was seen in Oncology clinic and laboratory evaluation was notable for potassium of 2.7 mmol/L prompting referral to the ED. Of note, during his visit with Oncology, the patient reported he had discontinued prednisone approximately six months prior as he remembered being told he no longer needed steroids by one of his physicians.In the ED, vital signs were notable for temperature 36 ° C, heart rate 102 beats per minute, and blood pressure 145/91 mmHg. Laboratory data was notable for potassium 2.8 mmol/L, Cr 0.8 mg/dL (baseline), and magnesium 1.7 mg/dL. He was given oral potassium chloride and admitted for telemetry monitoring.On admission, he was evaluated for adrenal insufficiency. Serum cortisol obtained at 6:30 AM was 1.1 ug/dL. Endocrinology was consulted and diagnosed abiraterone-induced adrenal insufficiency. He was started on oral hydrocortisone 15 mg every morning and 5 mg every afternoon and advised to follow up with Oncology and Endocrinology as an outpatient. Hypokalemia quickly resolved and remained stable without further supplementation after hydrocortisone was initiated.
Discussion: Abiraterone is commonly used in conjunction with ADT for men with metastatic castration-sensitive cancer who are unable to tolerate cytotoxic therapy. Abiraterone blocks the synthesis of androgens in the prostate tumor tissue, testes, and adrenal glands by inhibiting products of the cytochrome P450 17-alpha-hydroxysteroid dehydrogenase (CYP17) gene, including both 17,20-lyase and 17-alpha-hydroxylase. Due to its activity against 17-alpha-hydroxylase, abiraterone decreases cortisol synthesis leading to a compensatory increase in adrenocorticotropic hormone (ACTH). High levels of ACTH in turn cause increased mineralocorticoid production in the adrenal glands, which leads to hypertension and hypokalemia. Due to this toxicity profile, prednisone is coadministered with abiraterone to preserve cortisol production and reduce ACTH-mediated stimulation of the adrenal glands. In this case, careful medication reconciliation revealed that the patient’s self-discontinuation of prednisone precipitated hyperaldosteronism which caused hypokalemia and sustained ventricular tachycardia.
Conclusions: Medication reconciliation, including close review of discontinued medications and the reasons for discontinuation, is critical for the practicing hospitalist. Abiraterone, due to its mechanism of action, must be administered with corticosteroids to avoid hyperaldosteronism.