MON-485 - A Silent Collapse: HIV-Induced Adrenal Insufficiency - A Case Report

Adrenal insufficiency is defined by inadequate adrenocortical hormone production resulting from disruption at any level of the hypothalamic–pituitary–adrenal (HPA) axis. Although secondary causes such as chronic exogenous glucocorticoid use are most common, primary adrenal insufficiency may occur due to intrinsic adrenal pathology. HIV infection represents an uncommon etiology, with proposed mechanisms including direct adrenal involvement by opportunistic infections or malignancy, medication-related effects, and dysregulation of the HPA axis. In advanced HIV, these processes can impair cortisol synthesis and stress responsiveness, resulting in clinically significant adrenal dysfunction.

A 39-year-old man with multidrug-resistant HIV/AIDS on darunavir/cobicistat/emtricitabine/tenofovir/alafenamide (Symtuza) and fostemsavir, (Rukobia), chronic respiratory failure requiring tracheostomy, and percutaneous endoscopic gastrostomy tube dependence was admitted for recurrent septic shock. During hospitalization, he developed persistent and profound hypoglycemia, with glucose levels as low as 10 mg/dL, requiring escalating dextrose infusions, initiation of total parenteral nutrition with high dextrose content, and continuous D10 infusion. Similar hypoglycemic episodes had occurred during prior admissions, during which a random cortisol level was normal (18.8 µg/dL). Given recurrent hypoglycemia, endocrinology was consulted. A repeat morning cortisol level was 7.1 µg/dL (reference range 3.7–19.4 µg/dL). Cosyntropin stimulation testing demonstrated an inadequate cortisol response, with baseline cortisol of 8.5 µg/dL, 30-minute cortisol of 8.9 µg/dL, and 60-minute cortisol of 9.6 µg/dL. Adrenocorticotropic hormone level was 34 pg/mL (reference range 6–46 pg/mL). Stress-dose corticosteroid therapy with intravenous methylprednisolone 50 mg every 8 hours was initiated in the setting of ongoing sepsis, resulting in stabilization of blood glucose levels and hemodynamic status. Despite intervention, the patient’s condition deteriorated, and he was transitioned to comfort measures prior to death.

This case underscores HIV infection as a potential contributor to adrenal insufficiency through multifactorial mechanisms, including chronic immune activation with cytokine-mediated HPA axis suppression and direct adrenal injury from opportunistic infections. Although rare, recognition of this association is important, as corticosteroid therapy may rapidly reverse metabolic and hemodynamic instability in affected patients.

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