SAT-750 - A Hidden Diagnosis Behind Hypercalcemia in Hypoparathyroidism

A 51-year-old man with chronic kidney disease (CKD) stage IIIA and primary hypoparathyroidism for 25 years, managed with calcitriol and vitamin D3, presented with generalized body pain and constipation. He had multiple prior hospitalizations for both hypo- and hypercalcemia requiring frequent medication adjustments. On presentation, he was mildly hypotensive (96/62 mmHg) and clinically dehydrated; other vital signs were stable. Laboratory evaluation revealed severe hypercalcemia (calcium 17.5 mg/dL), hyponatremia (sodium 129 mmol/L), and acute kidney injury on CKD (creatinine 5.1 mg/dL; baseline 2.4 mg/dL).
Initial management included aggressive intravenous normal saline and calcitonin started. Detailed blood work obtained and laboratory studies showed elevated total protein (10.4 g/dL) with normal albumin (4.0 g/dL), raising concern for an underlying gammopathy, particularly given associated generalized and particularly back pain.
A hematologic workup was initiated. Serum and urine immunofixation revealed an IgA lambda monoclonal protein. A bone scan with SPECT was obtained, which showed multiple bilateral areas of contiguous anterior-lateral rib uptake in a vertical orientation, suspicious for prior trauma.
With supportive treatment, including intravenous fluids and calcitonin, the patient’s hypercalcemia, hyponatremia, and AKI resolved. Due to the suspicious clinical presentation and immunofixation findings, a bone marrow biopsy was performed.
Flow cytometric analysis of the bone marrow, gated on the CD138/CD38 (strong) population, identified a monoclonal, intracellular lambda light chain–restricted plasma cell population (kappa:lambda ratio < 0.01), accounting for approximately 41% of total marrow cellularity. These plasma cells were positive for cytoplasmic IgA heavy chains, partially positive for CD117, aberrantly positive for CD27, and negative for CD56. These findings were diagnostic of plasma cell myeloma.
Hypercalcemia is a common complication in patients with hypoparathyroidism receiving calcium and calcitriol therapy, and it is often presumed to be iatrogenic. However, like in our case, anchoring to the most apparent cause may delay recognition of alternative and clinically significant diagnoses. In clinical practice, there is a tendency to attribute findings to the most apparent or common cause. Nonetheless, it is essential to maintain a broad differential and evaluate for alternative etiologies.

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