Diagnostics & workup:
- Corrected calcium and ionized calcium: confirm hypercalcemia; correct total calcium for albumin
- PTH (intact): THE MOST IMPORTANT single test — elevated/inappropriately normal = PTH-dependent (PHPT, lithium, FHH); suppressed = PTH-independent (malignancy, vitamin D, granulomatous, thyrotoxicosis)
- If PTH elevated: 24-hour urine calcium/creatinine clearance ratio to distinguish PHPT (ratio > 0.02) from familial hypocalciuric hypercalcemia (FHH — ratio < 0.01; CaSR mutation, benign, no treatment needed)
- If PTH suppressed: PTHrP (malignancy), 25-OH vitamin D (exogenous D intoxication), 1,25-(OH)2 vitamin D/calcitriol (granulomatous disease, lymphoma), SPEP/UPEP (myeloma), TSH (thyrotoxicosis)
- Phosphate: low in PHPT (PTH promotes renal phosphate wasting); may be elevated in malignancy, renal failure
- Alkaline phosphatase: elevated with increased bone turnover (Paget, malignancy with bone metastases, PHPT with bone disease)
- Renal function: creatinine, eGFR (hypercalcemia can cause prerenal AKI; chronic PHPT can cause nephrocalcinosis and renal impairment)
- Parathyroid imaging (if PHPT confirmed): sestamibi scan + ultrasound for adenoma localization before surgery; 4D CT or PET/CT if initial imaging negative
Risk factors:
- Primary hyperparathyroidism (most common cause of outpatient hypercalcemia — prevalence 1-3 per 1000 in postmenopausal women)
- Malignancy (most common cause of inpatient hypercalcemia)
- Vitamin D supplementation excess (increasingly common with widespread supplementation)
- Granulomatous diseases: sarcoidosis, tuberculosis, fungal infections
- Thiazide diuretics (unmask or worsen PHPT)
- Lithium therapy (5% develop hypercalcemia)
- Immobilization (especially in Paget disease or young patients with high bone turnover)
- Milk-alkali syndrome (excessive calcium + antacid intake)
Management
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Prescribing & monitoring
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Takeaways
Additional clinical detail, exam hooks, and takeaways continue in the full lesson.
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