6761 PTH-independent Hypercalcemia Secondary to Severe Tophaceous Gout Bone Erosion

Disclosure: R.S. MacLeod: None. M.A. Cassetta: None. S.K. Majumdar: None. Introduction: Severe hypercalcemia associated with chronic tophaceous gout is extremely rare and usually related to elevated calcitriol secretion by inflammatory granulomatous lesions. Herein is a case where hypercalcemia appears to be mediated by excessive bone erosion in several gout lesions. Case: A 61-year-old man with history of advanced gouty arthropathy presented to the hospital with progressive weakness, lethargy and back pain. For the 3 months prior to presentation, he was noted to have worsening hypercalcemia of unknown etiology. He was not taking calcium or vitamin D supplements and had relatively low dietary calcium intake. He had a recent decrease in mobility and reduced fluid intake due to weakness and back pain in the past 6 months. On presentation, his corrected calcium was 16 mg/dL (8.8-10.2) with suppressed intact PTH of 10.4 pg/mL (16-77) and elevated uric acid at 9.0 mg/dL (2.7-7.3). Further evaluation revealed vitamin D25-OH was 28 ng/mL (30-100), PTH-rp was 21 pg/mL (14-27), and calcitriol was 49 pg/mL (18-72). Due to high normal ranges of PTH-rp and calcitriol, the differential included malignancy and sarcoidosis as possible drivers of hypercalcemia. Serum and urine protein electrophoreses showed no evidence for myeloma, and CT scans of the head, chest, abdomen and pelvis did not reveal malignancy but noted extensive arthropathy with soft tissue masses in the lumbar spine. Skeletal metastatic series showed erosive changes of the axial and appendicular skeleton consistent with inflammatory arthropathy. Two sets of biopsies performed of the L5 right pedicle mass revealed findings consistent with gouty tophus with some granulomas noted at the periphery. Serum CTx measurements were 2403 and 2802 pg/mL (87-345) on consecutive days indicating high bone turnover. Due to reduced renal function at the time, he was given 60 mg denosumab subcutaneously to treat his hypercalcemia. As his gout appeared to be the driver of his hypercalcemia, rheumatology was consulted and recommended uricase infusions for treatment. He had subsequent improvement of his corrected calcium to 10.8 mg/dL on the day of discharge. His calcium and uric acid later normalized and he experienced resolution of his gouty tophi with chronic uricase infusions, later transitioned to maintenance allopurinol. He has yet to receive other anti-resorptive treatments after the single dose of denosumab, now 3 years post treatment. Conclusion: Inappropriately high normal calcitriol in PTH-independent hypercalcemia should raise suspicion for granulomatous lesions or lymphoma facilitating extra-renal vitamin D conversion. In this case hypercalcemia appeared due to severe gouty arthropathy that resolved after treatment with uricase. It is likely that inflammation and granulomatous changes at the tophus-bone interface stimulated osteoclast activity and calcitriol production resulting in hypercalcemia. Presentation: 6/2/2024