THU579 Severe Hypokalemia: Is It Mineralocorticoid Excess Induced By Abiraterone Or Exogenous Hypercortisolism?

Abstract

Abstract Disclosure: D. Katwal: None. B.C. Barreto: None. J. Turner: None. D. James: Research Investigator; Self; Sanofi, Abbvie, Regeneron Pharmaceuticals. Introduction: Abiraterone is a CYP171A1 inhibitor used to treat metastatic, castration-resistant prostate cancer (CRPC). We report a case of severe hypokalemia in a patient with prostate cancer treated with abiraterone and prednisone, refractory after cessation of abiraterone, raising the concern for exogenous hypercortisolism. Case: A 69-year-old male with a history of locally advanced prostate cancer on Abiraterone 1 gm daily and prednisone 5 mg BID for a year presented to the local hospital ER with generalized weakness, diffuse paresthesia, and frequent falls. He was diagnosed with severe hypokalemia, renal wasting, metabolic alkalosis, and severe hypocalcemia. The patient's serum aldosterone was undetectable. CT scan of the pelvis was unremarkable for adrenal adenoma. Despite the undetectable aldosterone level, the patient's hypokalemia was initially attributed to an adverse effect of abiraterone, which was discontinued. He was discharged on potassium supplementation and eplerenone. However, he noted worsening symptoms, prompting him to visit our hospital the next day. On arrival, he was hypertensive. Lab showed potassium 2.9 mEq/L(3.6-5.0), bicarbonate 34mEq/L (21-31), creatinine 0.4 mg/dl (0.5-1.2), corrected calcium 6 mg/dl (8.4-10.2), ical 0.66 mmol/L (1.12-1.32), PTH 168 pg/ml (15-65) and vitamin D 25 OH 33 ng/ml (30-100). Oncology and nephrology were consulted to evaluate for abiraterone-causing hypokalemia. Nephrology suspected exogenous hypercortisolism, given his persistent electrolyte abnormalities off abiraterone for a week. He required aggressive potassium replacement of 240-360 mEq/day. Endocrinology was consulted to assist in tapering steroids, given the suspected exogenous hypercortisolism and risk of glucocorticoid-induced adrenal insufficiency. His biochemical profile improved over a week as we tapered his steroid to a maintenance dose of hydrocortisone. He was discharged with a plan to perform a cosyntropin test as an outpatient. Discussion: Abiraterone selectively and irreversibly inhibits CYP17A1 and subsequently inhibits androgen biosynthesis. Abiraterone treatment results in cortisol deficiency, with the compensatory elevation of ACTH level leading to hypokalemia, fluid retention, and hypertension due to excess mineralocorticoid. Steroids are co-administered with abiraterone to suppress ACTH and mineralocorticoid overproduction preventing adverse events. Our patient's persistent hypokalemia resulted from two distinct mechanisms of medical therapies used for his prostate cancer. Given his variable steroid status, a dexamethasone suppression test (DST) to establish biochemical hypercortisolism was not performed. This case highlights the importance of swiftly identifying endocrinopathies that may develop due to treatment from hormonal therapies that have become widespread in various fields of medicine. Presentation Date: Thursday, June 15, 2023