Hypercalcemia: Let PTH Organize the Workup

Excess calcium has several sources

Hypercalcemia can reflect increased bone resorption, enhanced gastrointestinal absorption, reduced renal excretion, or altered parathyroid regulation. Primary hyperparathyroidism and malignancy are major causes, but the broader differential remains important.

Recognize clinical impact

Polyuria, thirst, dehydration, constipation, weakness, confusion, and kidney dysfunction may occur. Severity depends on the calcium concentration, pace of change, symptoms, and comorbid disease; an acutely ill patient needs prompt assessment.

Confirm and measure PTH

Verify the calcium abnormality and consider ionized calcium when appropriate. PTH distinguishes a PTH-dependent pattern from appropriately suppressed PTH, which prompts evaluation for malignancy, vitamin D-related processes, medications, and other causes.

Tailor the second-line tests

Use phosphate, kidney function, vitamin D metabolites, PTH-related peptide, protein studies, and imaging according to the history and initial pattern. Avoid ordering every test indiscriminately or interpreting one biomarker as a stand-alone diagnosis.

Treat severity and mechanism

Restore volume when depleted and safe, consider rapid temporizing therapy for severe disease, and select cause-directed treatment. Antiresorptive choices depend on indication, kidney function, and risk, while glucocorticoids fit selected mechanisms.

Monitor the aftermath

Follow calcium, renal function, fluid status, and treatment-related electrolyte changes. Definitive treatment may require endocrine, oncology, or nephrology input. Loop diuretics are not routine calcium-lowering therapy in a patient who is volume depleted.

Self-check: After confirming hypercalcemia, explain how PTH determines the next branch of testing rather than ordering the entire differential at once.