Summary Immobilization-induced hypercalcemia is an uncommon cause of elevated calcium which is usually diagnosed following extensive systemic workup and exclusion of more common etiologies. Previously reported cases have largely described this phenomenon in adolescents and young adults a few weeks to months after the initial onset of immobilization. Metabolic workup tends to demonstrate hypercalcemia, hypercalciuria, and eventual osteoporosis. While the exact mechanism remains largely unclear, a dysregulation between bone resorption and formation is central to the pathogenesis of this disease. Decreased mechanical loading from prolonged bedrest tends to increase osteoclast induced bone resorption while promoting osteocytes to secrete proteins such as sclerostin to reduce osteoblast mediated bone formation. We describe the case of an 18-year-old male who was admitted following intraabdominal trauma. He underwent extensive abdominal surgery including nephrectomy resulting in initiation of dialysis. After 6 months of hospitalization, the patient gradually began developing uptrending calcium levels. Imaging and laboratory workup were unremarkable for any PTH-mediated process, malignancy, thyroid disorder, adrenal disorder, or infection. Workup did reveal significant elevated bone turnover markers which in combination with the clinical history led the physicians to arrive at the diagnosis of immobilization induced hypercalcemia. In order to prevent decreased rates of bone loss, the patient was administered denosumab for treatment. Hypocalcemia followed treatment expectedly and was repleted with supplementation via the patient’s total parenteral nutrition. Learning points Immobilization-induced hypercalcemia should remain as a differential diagnosis of patients with prolonged hospitalizations with hypercalcemia. Extensive workup of common etiologies of hypercalcemia should be considered prior to arriving at this diagnosis. Denosumab, while off-label for this usage, offers an effective treatment option for immobilization-induced hypercalcemia though it carries a risk of hypocalcemia especially among patients with renal disease.

Introduction: Hypophosphatemia is a recently recognized adverse effect of certain intravenous iron formulations. It was previously thought to be asymptomatic and transient, however it can cause severe hypophosphatemia associated with renal phosphate wasting. We present a case of severe hypophosphatemia following intravenous ferric carboxymaltose administration. Clinical Case: A 40-year-old female with history of iron deficiency anemia, Hashimoto’s hypothyroidism and multinodular goiter status post thyroidectomy and obesity status post gastric sleeve presents to the hospital due to dizziness, generalized weakness, bone pain and severe myalgia right after 2nd dose of 750 mg of ferric carboxymaltose administration. She received 1st dose of 750 mg of ferric carboxymaltose a week ago prior to the presentation. She was found to have severe hypophosphatemia with a phosphorus level 1.0 mg/dl (2.4 - 4.8 mg/dl), hypocalcemia with calcium level at 8.7 mg/dl, normal PTH at 40 pg/ml and normal 25-OH Vitamin D level at 59.1 ng/ml. The fractional excretion of filtered phosphate (FEPO4) was 19.5%, supporting renal phosphate wasting. She was hospitalized for 5 days and received intravenous phosphate 45 mmol on hospitalization day 1, 15 mmol on day 2 and 30 mmol on day 3. She was discharged on K-phos Neutral 250 mg TID, Calcium carbonate/Vitamin D3 600 mg/500 IU 2 tablets TID and Calcitriol 0.5 mcg daily. While she was taking K-phos Neutral, Calcitriol and Calcium carbonate/Vitamin D3, her phosphorous level was down to 1.3 mg/dl, which was 4 weeks after 1st dose of ferric carboxymatose administration. She presented to the ED and received intravenous phosphate 15 mmol. She is currently taking K-phos Neutral 250 mg QID, Calcitriol 0.5 mcg daily and Calcium carbonate/Vitamin D3 600 mg/500 IU 2 tablets TID. Her phosphorous levels ranged at 2.5 - 3.0 mg/dl. Her bone pain and myalgia have gradually improved. Conclusion: Clinician should be aware of the side effect of hypophosphatemia following ferric carboxymaltose administration. Recent studies showed that incidence of hypophosphatemia associated with intravenous iron administration was significantly higher in ferric carboxymatose group compared with either iron isomaltoside group or ferumoxytol group. The impact of severe hypophosphatemia should be considered when choosing an intravenous iron medication.