SAT-807 - When Biochemical Severity Mimics Malignancy: Hypercalcemic Crisis with Calcium 21 Mg/Dl from A Parathyroid Adenoma

Background: Hypercalcemic crisis is a rare endocrine emergency commonly caused by severe hypercalcemia due to malignancy. Extreme hypercalcemia exceeding 20 mg/dL due to a benign parathyroid adenoma is distinctly uncommon and poses diagnostic and therapeutic challenges, particularly when complicated by acute kidney injury (AKI). Parathyroid carcinoma should be considered if a patient with Primary Hyperparathyroidism (PHPT) develops severe hypercalcemia.

Clinical case: We present a 74-year-old woman with a known history of PHPT who developed progressive abdominal pain, nausea, vomiting, constipation, and worsening confusion over three weeks following myotomy for achalasia. She was disoriented during her initial presentation to the Emergency Department (ED) at her local hospital. Initial laboratory evaluation revealed severe hypercalcemia with calcium 20.6 mg/dL (corrected 21 mg/dL), markedly elevated parathyroid hormone (PTH) 1438 pg/mL, creatinine 1.66 mg/dL (eGFR 32 mL/min/1.73 m²), and severe hypokalemia. Given life-threatening hypercalcemia and acute kidney injury limiting bisphosphonate therapy, she was treated with aggressive intravenous fluids, calcitonin, and emergent hemodialysis. These efforts only partially reduced calcium levels, and encephalopathy did not improve much. PTH remained persistently elevated, and the patient was transferred to our facility for possible further management. Review of prior records showed a non-localizing parathyroid scan performed four months prior to the ED visit and a rapidly progressive biochemical disease. A 4D CT performed at our facility showed a right superior parathyroid mass measuring 1.4 × 1.1 cm, which was further confirmed by ultrasound, which showed a 2 cm parathyroid mass at the same location. The patient underwent parathyroidectomy with intraoperative PTH decline from 787 pg/mL to 71 pg/mL, followed by normalization of calcium and marked improvement in mental status. Final histopathology confirmed a benign parathyroid adenoma without features of malignancy.

Conclusion: This case demonstrates that benign PHPT can present with extreme hypercalcemia mimicking malignant disease. Proper hydration is especially important to prevent severe hypercalcemia in PHPT if definitive treatment with surgery is not opted for. In case of severe hypercalcemia crisis with encephalopathy, like in our case, all treatment options, including IV fluid, calcitonin, IV bisphosphonate (or denosumab), and hemodialysis, should be considered. If severe hypercalcemia is PTH-mediated, we should consider early surgical intervention, as parathyroid carcinoma could be a possible cause.

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