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Bone and Mineral Metabolism

MON-831 - Immobility-induced hypercalcemia in adults: time course, predictors, and clinical outcomes: A comprehensive systematic review

Monday, June 15, 2026
9:00 AM - 2:00 PM CT
Disclosure(s):
Sai Prasad, MBBS: No financial relationships to disclose
Background
Hypercalcemia secondary to prolonged immobility is a recognized but frequently underdiagnosed metabolic complication in adults who lose mechanical skeletal loading due to spinal cord injury, traumatic brain injury, critical illness, stroke, and major burns. However, its onset kinetics, biochemical predictors, and optimal management remain insufficiently characterized.

Objectives: To synthesize the available evidence on the time course, predictors, biochemical characteristics, management approaches, and clinical outcomes of immobility-induced hypercalcemia in adults.

Methods
A comprehensive systematic literature search was conducted in PubMed, Embase, and Scopus. Of the 2,471 records identified, 750 duplicates were removed, yielding 1,721 studies for title and abstract screening. Following the full-text review of 110 eligible studies, 17 studies met the final inclusion criteria, comprising 13 case reports, 2 case series, 1 retrospective cohort study, and 1 editorial review.

Results
Hypercalcemia typically develops within 4–12 weeks of immobilization, with onset as early as 10 days in patients with pre-existing renal impairment. The peak serum calcium levels ranged from 11.3 to 16.93 mg/dL (3.4–4.23 mmol/L). The hallmark biochemical profile comprised suppressed PTH, elevated bone resorption markers (CTx, NTX, TRACP5b), elevated urinary calcium, and low 1,25-dihydroxyvitamin D. Risk factors included younger age, high baseline bone turnover, complete immobilization, renal impairment, and CRRT with citrate anticoagulation, which can mask hypercalcemia. Intravenous bisphosphonates are the mainstay of treatment, and denosumab is used in advanced renal insufficiency or ESRD. Outcomes were generally favorable with timely antiresorptive therapy, although several patients developed acute kidney injury, recurrent episodes, or, in one case—bilateral atraumatic femoral fractures from undetected bone loss.

Conclusions
Immobility-induced hypercalcemia follows a predictable but under-recognized pathophysiology driven by uncoupled bone resorption without commensurate formation. Early recognition requires heightened clinical vigilance, systematic monitoring of ionized calcium (especially in hypoalbuminemic patients), and familiarity with masking phenomena, such as CRRT. Antiresorptive therapy with bisphosphonates or denosumab, complemented by aggressive hydration, is the cornerstone of treatment. Mobilization is both preventive and therapeutically essential.

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