ODP436 Adrenal Insufficiency After Combined Treatment of Itraconazole and Triamcinolone

INTRODUCTION: Adrenal insufficiency (AI) has been reported due to the use of budesonide and itraconazole. We report an unusual presentation of adrenal insufficiency from the use of triamcinolone and itraconazole. CLINICAL CASE: 46-year-old man with a history of NASH and alcoholic cirrhosis requiring liver transplant presented to ER with two weeks of progressive lower extremity weakness. He reported difficulty climbing stairs and getting up from a chair. He denied anorexia, nausea, vomiting, abdominal pain, or lightheadedness. He was treated with itraconazole for diffuse histoplasmosis for over one year and received one dose of intra-articular triamcinolone 40mg for shoulder pain 2 weeks prior to the hospital admission. Physical exam was significant for proximal weakness, ecchymoses on upper and lower bilateral extremities, mild truncal obesity, but no violaceous striae, moon facies, dorsocervical fat pad or supraclavicular fullness. Laboratory evaluation was notable for sodium 129 mEq/L (n: 135-145), potassium 5.9 mEq/dl (n: 3.5-5), albumin 2.9 g/dl (n: 3.5-5) and glucose 345 mg/dl (n: 70-140), ACTH of 6 pg/ml (6-20) AM cortisol of <1 ug/dl (n: 4-20), aldosterone <1 ng/dl (n: 3-16), and plasma renin activity (PRA)20.54 ng/mL/h (n: 0.25-5.82). Serum cortisol increased to 3.4 ug/dl at 60 minutes of cosyntropin stimulation test, consistent with adrenal insufficiency. Synthetic glucocorticoid panel detected triamcinolone. Patient was discharged on hydrocortisone and fludrocortisone with marked clinical improvement. Abdominal MRI 3 months after admission did not show any adrenal involvement by histoplasmosis. Fludrocortisone was slowly titrated off and only hydrocortisone continued. Repeat evaluation 6 months after last triamcinolone injection demonstrated recovery of HPA axis with peak cosyntropin stimulation cortisol level 16.3 ug/dL (assay by Abbott Alinity) and recovery of renin/angiotensin/aldosterone axis (AM aldosterone 7 ng/dl, renin 2 ng/ml/h). Repeat synthetic glucocorticoid testing confirmed clearance of triamcinolone. CONCLUSION: Itraconazole is CYP3A inhibitor that has been shown to decrease the metabolism and clearance of different corticosteroids. While our patient's lab results supported a diagnosis of AI, it was unclear if the etiology was primary (PAI) or central AI (CAI). The Na+, K+, aldosterone and PRA levels support a diagnosis of PAI; whereas the suppressed ACTH level supports CAI. We believe that our patient had an atypical presentation of both PAI due to histoplasmosis and CAI due to itraconazole/triamcinolone. This confounding picture can potentially be explained by an underlying PAI that may have been masked and exacerbated by the HPA axis suppression of the itraconazole/triamcinolone combination. Presentation: No date and time listed