Abstract

Abstract Background Central adrenal insufficiency from drug-drug interaction between steroids and HIV anti-retroviral medications is a well-documented phenomenon in the literature, but in clinical practice making this diagnosis can prove challenging. Clinical Case 58-year-old woman with well-controlled HIV on dolutegravir and cobicistat/darunavir, type 2 diabetes mellitus, and chronic kidney disease presented to our emergency department with 3 days of polyuria, polydipsia, headaches, nausea, and decreased appetite. She also noticed that her glucose readings have been much higher than usual. 5 days prior to presentation, she received a 40 mg triamcinolone acetonide injection into her right subacromial bursa for chronic shoulder pain. For diabetes, she had been on the same dosage of weekly dulaglutide with good control. Initial laboratory evaluation revealed elevated serum glucose of 763 mg/dl (70 - 140 mg/dL) without an elevated anion gap, sodium of 124 mEq/L (135 - 145 mEq/L) and potassium of 5.9 mmol/L (3.6 - 5.2 mmol/L). Morning cortisol was sent as part of the workup for hyponatremia and returned low at 1.2 ug/dL (4 - 20 ug/dL). A 250 mcg cosyntropin stimulation test was performed, with baseline cortisol at 1.3 ug/dL and one-hour post-stimulation cortisol of 8.8 ug/dL. Pre-stimulation ACTH was < 5. 0 pg/mL (10 - 60 pg/mL). A synthetic glucocorticoid panel were sent on the 11th day after her injection and detected triamcinolone acetonide at 3.3 mcg/dL (cutoff: 0.1 mcg/dL) in urine and 0.85 mcg/dL (cutoff: 0.1 mcg/dL) in serum. She was diagnosed with iatrogenic adrenal insufficiency from intra-articular triamcinolone injection, the effect of which had been potentiated by her HIV medications cobicistat and dolutegravir (both CYP3A4 inhibitors). She was started on hydrocortisone and experienced improvement in appetite and fatigue. A plasma renin activity assay was elevated at 7.66 ng/mL/h (0.25 - 5.82 ng/ml/h) with 15 ng/dL of aldosterone (3 - 16 ng/dL). While awaiting the ACTH result, we discussed the possibility of primary adrenal insufficiency given persistent hyponatremia despite improved glucose control. However, given recent normal cross-sectional abdominal imaging, the history of steroid exposure, and lack of opportunistic infections in the past, central adrenal insufficiency remained the leading diagnosis. Further workup, including urine anion gap, eventually determined the cause of her hyponatremia to be a type 4 RTA likely related to her longstanding history of diabetes. The patient was discharged home on hydrocortisone with plan for repeat stimulation test in 6 weeks. Conclusion 1. Keep primary adrenal insufficiency in mind in a patient with HIV who presents with hyponatremia and low cortisol. 2. Steroid injections carry risks of significant hyperglycemia and iatrogenic adrenal insufficiency in patients receiving cobicistat and integrase inhibitor. Presentation: No date and time listed

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