Abstract: FR-PO0598
An Antifungal Tradeoff: A Case of Adrenal Insufficiency from Long-Term Fluconazole Treatment of Coccidiomycosis
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Lopez, Yvette Y, Abrazo Health Care, Phoenix, Arizona, United States
- Moasser, Amir H., Arizona Kidney Disease and Hypertension Centers, Glendale, Arizona, United States
- Santos, Peter W., Arizona Kidney Disease and Hypertension Centers, Glendale, Arizona, United States
Introduction
Azole antifungal therapy has been mainstay treatment of various systemic mycoses and can cause adrenal dysfunction. While posaconazole and itraconazole can cause adrenal steroidogenesis leading to pseudohyperaldosteronism, ketoconazole is most frequently reported azole to cause primary adrenal insufficiency by inhibiting 11b-hydroxylase and 17a hydroxylase enzymes responsible for the production of cortisol. There are case reports of fluconazole induced adrenal insufficiency in critical ill setting. We report a case of adrenal insufficiency associated with long term use of high dose fluconazole.
Case Description
A 48-year-old male with hypertension presented to our hospital for evaluation of hyperkalemia based on an outpatient potassium (K) result of 7 mEq/L. His vitals were stable and physical exam was unrevealing. He was diagnosed with coccidioidomycosis 5 years ago. He was started on fluconazole 800 mg daily and decreased to 600 mg daily 3 years later. Admission labs were notable for Na 131 mEq/L, K 6.2 mEq/L, CO2 17 mEq/L with AG of 11. His renal function was normal with Cr 0.93 mg/dL with eGFR 101 ml/min. He received insulin, dextrose, calcium gluconate, albuterol inhaler, and sodium zirconium cyclosilicate for his hyperkalemia. Cosyntropin stimulation test revealed limited response to ACTH and cortisol results were 4.8 ug/dl at baseline, 7.4 ug/dl at 30 min, and 7.8 ug/dl at 60 min. Phlebotomy missed ACTH level. After clinical diagnosis of primary adrenal insufficiency, hydrocortisone 10 mg BID and fludrocortisone 0.1 mg was inititated daily. His electrolyte and metabolic profiles improved on the day of discharge – Na 136, K 4.4, CO2 22. Two months later, he was readmitted with hyperkalemia K 7.0 and metabolic acidosis CO2 12. Prior to his hospitalization, he stopped taking hydrocortisone and fludrocortisone since hyperkalemia resolved from his last outpatient lab. Both medications were resumed resulting in normalization of hyperkalemia and metabolic acidosis.
Discussion
Fluconazole is a weak steroidogenesis inhibitor compared to ketoconazole. Chronic exposure to high doses of fluconazole could potentially impair cortisol synthesis through inhibition of steroidogenic enzymes leading to primary adrenal insuffiency. We believe it is important to bring awareness of this underrecognized risk to prevent delayed diagnosis and management.