SAT228 Denosumab Associated Severe Hypocalcemia Due To Vitamin D Deficiency In A Patient With Undiagnosed Primary Hyperparathyroidism

Disclosure: S. Bendaram: None. P.J. Bhatt: None. V. Kantorovich: None. Background: The Human monoclonal antibody, Denosumab is a widely used antiresorptive therapy for Osteoporosis, which in the presence of risk factors can lead to hypocalcemia. We present an interesting case of severe and prolonged hypocalcemia due to Denosumab therapy, due to Vitamin D deficiency from malabsorption, despite the presence of undiagnosed Primary Hyperparathyroidism (PHPT). Case Presentation: 74-year old white female with a history of Crohn’s disease s/p ileostomy, Osteoporosis on Denosumab, Seizure disorder on Divalproex, and Parkinson’s disease presented to the ED for worsening altered mental status and decreased oral intake for at least 2 weeks prior to admission. On presentation, she was alert, oriented to person only, complaining of body aches. She was on no vitamin D supplements. Vital signs were unremarkable except for low BMI of 17.05 kg/m2. Physical exam revealed a chronic upper extremity tremor and a new facial mouth tremor associated with bruxism. Chvostek and Trousseau signs were negative, however this was after 1 dose of IV calcium gluconate in the ED. On presentation, initial labs revealed total calcium of 5.3 mg/dL [8.7-10.5], Albumin 4.7 g/dL [3.4-4.8], Magnesium 1.2 mg/dL [1.6-2.7], creatinine 1.5 mg/dL [04-1.1] (baseline 1.0). Further testing showed ionized calcium of 0.56 mmol/L [1.17-1.33], 25 Hydroxy Vitamin D 9 ng/mL [30-100], PTH 777 pg/mL [15-65] and phosphorus 3.6 mg/dL [2.7-4.5]. She was treated with IV calcium gluconate, 50,000 IU weekly vitamin D3 and calcium citrate 950mg oral BID, followed by which her total calcium went up to 12 mg/dl, with ionized calcium elevated at 1.36 mmol/L, while herPTH levels stayed inappropriately normal at 55 pg/ml. On the day of discharge, 25-OH-Vitamin D was 15 ng/dl, PTH 222 pg/ml and ionized calcium 1.07 mmol/L, when she was alert, oriented, with resolution of bone pains. Conclusion: Hypercalcemia in PHPT is from activation of osteoclasts and when these cells are inhibited by antiresorptive therapy, intestinal absorption will remain the primary source of plasma calcium levels. This explains the severe and prolonged hypocalcemia caused by Denosumab owing to its mechanism of action and long elimination half life, in our patient with Vitamin D deficiency on the background of malabsorption, despite a combination of primary and secondary elevation of PTH. Careful baseline assessment of calcium and Vitamin D levels, along with adequate supplementation and regular monitoring should be undertaken in all patients treated with Denosumab to avoid this. Presentation: Saturday, June 17, 2023