SAT-760 - PTH-independent Hypercalcemia Uncovering Chronic Use of an Over-the-counter Supplement

Background: PTH-independent hypercalcemia occasionally develops during the course of a patient’s hospital stay and is most frequently caused by prolonged immobilization. We hereby present the case of a patient who developed severe PTH-independent hypercalcemia several days into his hospitalization. Identifying the underlying etiology was delayed by the patient not disclosing, and the treatment team not identifying, the use of exogenous glucocorticoids in a timely manner.

Case: A 43-year-old male with past medical history of severe deforming tophaceous gout, primary hypothyroidism, and prior stroke presented with an acute gout flare of multiple joints and acute renal insufficiency necessitating inpatient admission for pain control. His albumin-adjusted serum calcium (which had previously been normal) was 10.6 mg/dL on admission, decreased to 9.4 mg/dl with IV hydration, but then progressively increased over the subsequent 10 days, peaking at 14.2 mg/dL despite aggressive intravenous fluids. Evaluation of hypercalcemia was notable for appropriately suppressed serum PTH (4.9 pg/ml), low 25-hydroxy vitamin D (13.6 ng/mL), low 1,25-dihydroxy vitamin D (9.2 pg/mL), and SPEP showed no monoclonal spike. Further workup revealed undetectable morning cortisol levels, low ACTH (6 pg/mL), and low DHEAS (10 mcg/dL). On further questioning, the patient eventually disclosed chronic use of Ardosons, an over-the-counter supplement containing betamethasone that he was buying from Mexico to treat his chronic arthritis, and which was not continued during the admission. Secondary adrenal insufficiency due to withdrawal of exogenous glucocorticoids was diagnosed. Hydrocortisone replacement was initiated at slightly supra-physiologic doses, resulting in a rapid normalization of serum calcium levels (within 36 hours). The patient was discharged on maintenance hydrocortisone therapy with long-term maintenance of normocalcemia.

Discussion: Hypercalcemia is an uncommon but recognized manifestation of adrenal insufficiency. Proposed mechanisms include volume depletion with increased proximal tubular calcium reabsorption, reduced glomerular filtration rate, and loss of glucocorticoid-mediated inhibition of bone resorption. This case highlights the diagnostic importance of assessing the pituitary-adrenal axis in unexplained PTH-independent hypercalcemia. Detailed medication and supplement history is critical, as some unregulated products may contain potent glucocorticoids. Recognition of this reversible cause allows prompt correction with glucocorticoid replacement.

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