SAT-773 - Calcium Crash: A Case of Severe Hypocalcemia after Denosumab and Intravenous Iron

Background
Severe hypocalcemia can occur in patients with chronic kidney disease (CKD), Vitamin D deficiency and after the antiresorptive therapy interruption. Early recognition is essential, even in the absence of classic neuromuscular symptoms.
Case Presentation
An 83-year-old woman with osteoporosis, hypothyroidism, gastroesophageal reflux disease, CKD, prior gastric bypass surgery presented to the hospital for dizziness and fall resulting in left transcondylar distal humerus fracture. Further evaluation showed calcium 5.6mg/dL (8.2-10.1mg/dL), albumin 3.8g/dL (3.5-5.2 g/dL), phosphorous 3.5 mg/dL (2.2-5.5mg/dL), creatinine 1.2mg/dL (0.4-1.2 mg/dL) and parathyroid hormone 653.3pg/ml(24-85pg/ml). She had no neuromuscular symptoms and no electrocardiogram changes. Patient had received Denosumab from her primary care provider 9 days prior to her fall and had been on this medication for about 4 years. She received bolus doses of intravenous (IV) calcium gluconate and was restarted on her home dose of oral calcium 500mg once a day. Calcium initially increased from 5.6 mg/dL to 6.2 mg/dL (8.2-10.1mg/dL). During her stay, she received 5 days course of IV iron sucrose 200mg daily for persistent anemia despite oral iron supplementation. After iron sucrose started the patient's phosphorus decreased from 3.5mg/dL to 2.2 mg/dL (2.2-5.5 mg/dL) and calcium decreased from 6.2mg/dL to 5.5 mg/dL (8.2-10.1 mg/dL). IV iron sucrose stopped and the patient started on IV calcium infusion and more aggressive oral calcium regimen. Patient's phosphorus improved once the iron sucrose stopped and calcium improved rapidly with calcium infusion. She was transitioned off infusion and continued oral regimen, being discharged on calcium citrate 1900mg three times a day.
Conclusion
This is a case of severe hypocalcemia driven by denosumab therapy and exacerbated by IV iron sucrose, Prompt discontinuation of iron sucrose, initiation of IV calcium infusion, and oral calcium supplementation resulted in rapid improvement. IV iron can acutely suppress serum calcium and phosphate levels through fibroblast growth factor-23 (FGF-23) mediated mechanisms. Ferrous carboxymaltose and iron sucrose are more commonly associated with hypophosphatemia and hypocalcemia, but this case highlights that any formulation of IV iron can cause electrolyte imbalances.

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