A 65-year-old woman has serum Ca²⁺ 11.8 mg/dL, phosphate 1.9 mg/dL, PTH 95 pg/mL (elevated), and 24-hour urine calcium 450 mg. Alkaline phosphatase is mildly elevated. This laboratory profile is most consistent with which condition, and what is the primary mechanism of hypercalcemia?
- A Primary hyperparathyroidism; PTH increases osteoclastic bone resorption, renal tubular Ca²⁺ reabsorption, and 1,25-(OH)₂ vitamin D synthesis, all raising serum Ca²⁺ while lowering phosphate ✓
- B Humoral hypercalcemia of malignancy; PTHrP mimics PTH but causes PTH suppression, not elevation
- C Vitamin D toxicity; causes hypercalcemia but PTH should be suppressed, not elevated
- D Familial hypocalciuric hypercalcemia (FHH); PTH is elevated but urinary calcium is characteristically low, not high
Correct answer: A. Primary hyperparathyroidism; PTH increases osteoclastic bone resorption, renal tubular Ca²⁺ reabsorption, and 1,25-(OH)₂ vitamin D synthesis, all raising serum Ca²⁺ while lowering phosphate
Explanation
The combination of hypercalcemia with simultaneously elevated (non-suppressed) PTH defines primary hyperparathyroidism (most commonly due to parathyroid adenoma). PTH acts on bone (stimulates osteoclasts via RANK-L), kidney (promotes Ca²⁺ reabsorption in DCT, phosphate excretion in PCT, and upregulates 1α-hydroxylase), and indirectly increases GI Ca²⁺ absorption via calcitriol. The resulting hypercalcemia with hypophosphatemia and elevated urinary calcium is the classic pattern. In FHH, urinary Ca²⁺ is low (calcium-to-creatinine clearance ratio < 0.01).
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
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