Reversible Adrenal Hyperplasia Associated with Chronic Etomidate Use: A Case Report with 3-Year Radiological Follow-Up

Abstract Background: Etomidate, a commonly used intravenous anesthetic, is known to reversibly inhibit adrenal 11β-hydroxylase (CYP11B1). Illicit electronic cigarettes containing etomidate have emerged in some regions, and chronic inhalation has been associated with acquired adrenal hyperplasia. However, the long-term reversibility of etomidate-induced adrenal hyperplasia after drug cessation has not been documented in the literature.

Case presentation

We report a 33-year-old male patient who presented with recurrent fatigue, after approximately 10 years of 4-5 times per week etomidate-containing e-cigarette use. Laboratory evaluation revealed hypokalemia (serum K⁺ 3.37 mmol/L), normal morning cortisol (9.66 μg/dL), elevated adrenocorticotropic hormone (ACTH) (322.00 pg/mL), and normal aldosterone-to-renin ratio. Computed tomography demonstrated bilateral adrenal thickening (9.3mm on the right, 9.5 mm on the left). Genetic testing excluded CYP11B1 and CYP21A2 mutations, supporting an acquired etiology. The patient was advised to discontinue etomidate use. At the 3-year follow-up, the patient remained abstinent. Repeat CT imaging showed largely resolution of adrenal hyperplasia, with adrenal thickness reduced to 3.9-4.3 mm bilaterally, and biochemical parameters returned to normal range.