SAT-435 - A Case of Abiraterone-Related Adrenal Insufficiency with Mineralocorticoid Excess

Introduction:
Adrenal insufficiency may occur secondary to impaired cortisol synthesis resulting from inhibition of steroidogenesis. Abiraterone, an androgen biosynthesis inhibitor used in the treatment of metastatic castration-resistant prostate cancer, irreversibly inhibits 17α-hydroxylase and 17,20-lyase, leading to cortisol deficiency and compensatory ACTH elevation. This dysregulation can promote mineralocorticoid excess. We report the case of an 80-year-old patient who developed adrenal insufficiency complicated by hypertensive crisis in the setting of abiraterone therapy.

Case Description:
An 80-year-old male with a history of metastatic castration-resistant prostate cancer presented to the emergency department with generalized weakness, abdominal pain, fatigue, and shortness of breath. On admission, he was hypotensive and had evidence of acute kidney injury and hyperkalemia. Further history revealed that he had been started on abiraterone and relugolix six months earlier, in combination with prednisone 5 mg daily. He had recently completed antibiotic treatment for a urinary tract infection but did not demonstrate clinical improvement.

Given his presentation, adrenal insufficiency was suspected, and an early-morning cortisol level was obtained after holding his home prednisone for 48 hours. The cortisol level was markedly low ( < 0.4 µg/dL). Endocrinology was consulted, and the patient was initiated on stress-dose glucocorticoids, with rapid clinical improvement. The steroid dose was gradually tapered during his hospital stay to a physiological dose. Several days later, he developed hypertension, requiring escalation of his antihypertensive regimen. The patient was followed closely in the endocrinology clinic and continued to experience symptoms while receiving prednisone 5 mg daily. The dose was subsequently increased to 5 mg twice daily, resulting in significant clinical improvement and normalization of blood pressure.

Conclusion:
Abiraterone inhibits steroidogenesis and is associated with the development of adrenal insufficiency, necessitating concomitant glucocorticoid therapy. Prednisone is preferred over hydrocortisone in this setting due to its relative superior ability to suppress ACTH and reduce the risk of mineralocorticoid excess. Doses higher than physiologic replacement may be required. Careful clinical assessment remains essential, as symptom burden continues to be the primary guide for glucocorticoid dose adjustment.

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