Immobilization-induced hypercalcemia in a patient with renal failure. (4th October 2021)

• Record Type: Journal Article
• Authors: Gandhi, Anand; Mortensen, Mike; Sunny, Sonie; Techathaveewat, Pawarid; Targovnik, Jerome; Alsayed, Mahmoud
• Is Part Of: Endocrinology, diabetes & metabolism case reports. (2021)
• Publication Date: 2021-10-04
• Subjects: Adult -- Male -- Black - other -- United States; Parathyroid -- Bone; New disease or syndrome: presentations/diagnosis/management -- October -- 2021; Endocrinology -- Periodicals; Diabetes -- Periodicals; Diabetes Mellitus; Endocrinology; Diabetes; Endocrinology; Case Reports; Periodicals; Periodicals; 616.4
• DOI: 10.1530/EDM-21-0086
• Languages: English
• ISSNs: 2052-0573

Abstract

Abstract : 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.