PMON283 A CASE OF INHALED FLUTICASONE INDUCED ADRENAL INSUFFICIENCY

Abstract

Abstract Inhaled glucocorticoids (ICS) are recommended in all patients with persistent asthma. While relatively safe, ICS can occasionally cause systemic side effects including adrenal suppression, bone loss, and cataract formation. We describe a 53-year-old woman with adrenal insufficiency secondary to inhaled fluticasone. A 53-year-old woman was referred for evaluation of an incidental 5.5×2.7 cm left adrenal mass discovered on CT chest when she was hospitalized for an asthma exacerbation. She had asthma since the age of 20 and had intermittently been on oral steroids which were tapered off several months prior to her evaluation. Medications included fluticasone (230-21mcg/actuation inhaler) HFA 2 puffs twice daily, azithromycin, azelastine, calcium carbonate, cholecalciferol, esomeprazole, guaifenesin, magnesium, and montelukast. On exam vital signs were: BP 128/88, HR 95, BMI 41.13 kg/m2. She was obese with left > right supraclavicular fullness, mild dorsocervical fullness, slightly thinned skin, but no striae or proximal muscle weakness. Labs were initially sent to evaluate for an adrenal incidentaloma: A random morning (8 AM) cortisol was <0.5 mcg/dL (6-18 mcg/dL), plasma ACTH was 6pg/ml (7.2-63.3 pg/mL), 24 hour free urinary cortisol: < 1mcg/24 hours (2500 ml/ 24hr urine, urine creatinine 1.66g/24 hours). Urine and plasma metanephrines and normetanephrines were negative. FSH and LH were normal. A 250 mcg cosyntropin stimulation test was done showing a baseline cortisol of <0.5 mcg/dL and ACTH <3.0 pg/mL, cortisol levels of 2.7 mcg/dL and 3.2 mcg/dL at 30 and 60 minutes, respectively. Pituitary MRI was normal. She was diagnosed with adrenal insufficiency likely caused by an exogenous steroid. Since she had been off oral steroids for several months urinary steroid testing was performed revealing an elevated fluticasone metabolite: Fluticasone 17β-carboxylic acid >10,000 pg/nL (nl < 10 pg/nL). Hence inhaled fluticasone was determined to be the cause. Similar findings have been described in patients with HIV on anti-retroviral therapy (ART) where metabolism of inhaled steroids can be impaired resulting in hypothalamic-pituitary-adrenal suppression. Our patient was not on ART but may have a genetic variant resulting in delayed steroid clearance or enhanced susceptibility to HPA suppression, though fluticasone is known to accumulate in adipose tissue. She stopped fluticasone and several days later repeated urine testing revealing a urine Fluticasone 17β-carboxylic acid level of 96 pg/nL, two weeks later inhaled budesonide was initiated and over the course of three months her ACTH increased from 3.3 to 18.3 to 26.3 (pg/mL) and cortisol rose slightly from 0.9 to 3.2 to 3.7 mcg/dL. Conclusion Awareness of the potential systemic side effects of inhaled corticosteroids is important and patients should be kept on the lowest effective dose. Conversely, in the evaluation of patients with secondary adrenal insufficiency the possibility of inhaled corticosteroids playing a causative role should be considered. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.