6734 Hypercalcemia Of Immobilization (HCOM) Responding To COVID Treatment: A Mere Coincidence Or More?

Disclosure: R. Shafiq: None. A. Javed: None. A. Haider: None. A paraplegic patient who developed HCOM and subsequently received steroids for COVID-19 pneumonia with improvement in calcium levels. After completing steroid treatment his hypercalcemia relapsed and received IV bisphosphonates with normalization of calcium levels. Case: A 58-year-old male who became paraplegic after a fall in August, of 2022. In October 2022, during admission for sepsis related to an Indwelling foley catheter, his corrected calcium was 12 mg/dl. Despite IV hydration calcium remained elevated. In December 2022, the patient was readmitted for COVID-19 pneumonia & received Decadron 6 mg daily. On admission calcium was 13.2mg/dl with pertinent labs of PTH 4 (8.5-77 pg/ml), Vitamin D 1,25 was 31 (18-72 pg/ml), and PTHrp was normal. C- telopeptide was 1068 (87-345 pg/ml) which improved to 877 pg/ml after completing Decadron for COVID pneumonia. Also, Calcium transiently improved from 13.2mg/dl on admission to 9.8 mg/dl. Calcium levels were noted to be elevated again up to 14 mg/dl a month after discharge. February 2023, after IV bisphosphonate infusion corrected calcium normalized. In June 2023 calcium was high again at 14.4 mg/dl. IV hydration with a brief 3-day course of dexamethasone before receiving the second dose of zoledronic normalized corrected calcium. Discussion: Dysregulation in bone formation & resorption is due to the absence of mechanical stress in prolonged bed rest which is essential for bone remodeling. Lack of mechanical stress results in increased secretion of Sclerostin, a protein secreted by mature osteocytes that inhibits the Wnt signaling pathway resulting in increased bone resorption & decreased bone formation. Steroids reduce sclerostin production causing an improvement in calcium levels due to reduced bone resorption. His C telopeptide level was 1068 pg/ml) which improved to 877 pg/ml after steroids also supported Sclerostin-mediated bone resorption as a cause of hypercalcemia. Antiresorptive agents like IV bisphosphonates and Denosumab especially in patients with renal failure are the first-line treatments for HCOM. He did require an additional dose of IV zoledronic acid 4 months after the initial dose to maintain normocalcemia. Conclusion: HCOM is managed by physical therapy, IV hydration, and IV bisphosphonates. Since hypercalcemia of immobilization is a sclerostin-mediated bone resorption process, a short course of steroids or the use of anti-sclerostin monoclonal antibody Romosozumab can be a reasonable treatment consideration however more research is needed for that. Presentation: 6/2/2024