Hypercalcemia: A Metabolic Disorder with Wide Range of Side Effects-An Updated Review for Healthcare Professionals | ||
| Egyptian Journal of Chemistry | ||
| Volume 68, Issue 13, December 2025, Pages 1185-1194 PDF (246.22 K) | ||
| Document Type: Review Articles | ||
| DOI: 10.21608/ejchem.2025.406530.12082 | ||
| Authors | ||
| Abdulrahman Abdullah Aljadid* ; Aishah Abduh Mohammed Hazazi; Bashayer Ali Alshehri; Sara Yahya Sharbib; Ebtesam Hathal Alotaibi; Hind Aedh Alotaibi; Mariam Wadi Alanazi; Elaf Mohmmad Alashhab; Razan Rashed Bin Thari; Mansour Ali Alqahtani; Raghad Binbaz Alqahtani; Maha Fuhied Alharthi; Khaled Mohammed Alqattan; Wael Ibrahim Alghanim; Fatema Rafia Alelaiwi; Hala Rajeh Alqahtani | ||
| Ministry of National Guard, Saudi Arabia | ||
| Abstract | ||
| Background: Hypercalcemia is a prevalent biochemical abnormality with heterogeneous etiologies and system-wide consequences. Its clinical impact spans incidental laboratory findings to life-threatening cardiovascular and neurologic instability. Aim: To provide an updated, practical synthesis for healthcare professionals covering pathophysiology, epidemiology, diagnostic pathways, management options, and team-based care of hypercalcemia. Methods: Narrative review of established concepts summarized into a clinician-oriented framework, emphasizing the parathyroid hormone (PTH) decision node, severity grading, targeted investigations, and evidence-based treatments, with attention to patient education and follow-up. Results: Calcium homeostasis is governed primarily by PTH and vitamin D, with calcitonin as a minor counter-regulator in adults. Most cases derive from primary hyperparathyroidism or malignancy. Severity stratification (mild 10.5–11.9 mg/dL; moderate 12.0–13.9 mg/dL; crisis 14.0–16.0 mg/dL) guides urgency. A suppressed versus inappropriately normal/elevated PTH separates PTH-independent from PTH-mediated causes, prompting tests such as 24-hour urinary calcium, vitamin D metabolites, PTH-related peptide, serum and urine electrophoresis, thyroid studies, metanephrines, and imaging for malignancy or parathyroid disease. Initial treatment prioritizes volume repletion, electrolyte correction, and rapid calcium lowering with calcitonin, followed by durable antiresorptives (zoledronic acid, pamidronate, or denosumab). Etiology-specific measures include parathyroidectomy for eligible primary hyperparathyroidism, glucocorticoids for calcitriol-mediated disease, cinacalcet when surgery is unsuitable, and dialysis for severe, refractory cases. Interdisciplinary follow-up mitigates recurrence and complications. Conclusion: Etiology-directed, severity-informed care anchored to the PTH decision point enables efficient management that improves safety, reduces recurrence, and aligns with patient goals | ||
| Keywords | ||
| hypercalcemia; primary hyperparathyroidism; malignancy-related hypercalcemia | ||
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