(CSEMP050) LYTIC BONE LESIONS? CALL ENDOCRINOLOGY!

Abstract: Case
A 58-year-old male patient with a history of nephrolithiasis was admitted to Oncology with a 2-month history of right thigh pain. Imaging showed multiple lytic lesions in the proximal femurs, vertebral bodies, and pelvis concerning for multiple myeloma vs. metastatic disease. Initial ionized calcium was 2.35 mmol/L (normal upper limit: 1.28 mmol/L). PTH was 173 pmol/L (normal upper limit: 6.9 pmol/L). Parathyroid carcinoma was suspected given the degree of hypercalcemia, PTH elevation, and apparent bone metastases.

A parathyroid scan indicated a possible left parathyroid mass that was surgically removed and found to be a benign 3.9 cm left superior parathyroid adenoma. He underwent right femur intramedullary nail fixation for impending fracture. Pathology of bone fragments noted benign degenerated bone with focal remodeling and fibrosis. The patient developed hemorrhagic shock with 3 liters of surgical blood loss, and upon transfer to the ICU, required pressor support.

Following the left parathyroidectomy, PTH normalized to 2.3 pmol/L. The patient then developed severe hypocalcemia (ionized calcium 0.79 mmol/L, normal lower limit: 1.14 mmol/L) with high PTH (13.9 pmol/L), and was started on calcitriol (highest daily dose 3 mcg) and calcium supplementation (highest elemental calcium daily dose 6000 mg).

After a 2-month hospital admission, he was discharged home, and within a few weeks was only on elemental calcium dose of 1000 mg twice daily.

Discussion
The bony lytic lesions at presentation raised great concern for multiple myeloma or bone metastases. Endocrinology assessment revealed primary hyperparathyroidism with elevated PTH (almost 25 times the upper limit of normal) alarming for parathyroid carcinoma, which can lead to bone metastases and/or osteitis fibrosa cystica (OFC).

Pathological analysis revealed this was a parathyroid adenoma with OFC. The right femur lesion bled extensively intra-operatively, and this is not uncommon with surgical intervention for OFC lesions which tend to be very vascular. Furthermore, OFC is a risk factor for developing hungry bone syndrome characterized by prolonged hypocalcemia post-parathyroidectomy, which was the case in our patient.

In conclusion, in the setting of critically severe hypercalcemia and elevated PTH, OFC should not be forgotten as a cause of lytic lesions. Coordinated care with Oncology, ENT, Orthopedic Surgery and Endocrinology was vital to determining the etiology of this patient’s presentation.