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Difficulty: MediumInterpreting Laboratory Results

Match each of the following sets of serum biochemical findings (calcium, phosphorus, and intact parathyroid hormone) with the diagnostic entity it most characteristically represents.

(Reference ranges: Serum calcium 8.4-10.2 mg/dL, Serum phosphorus 2.5-4.5 mg/dL, Intact PTH 15-65 pg/mL)

  • Calcium 11.5 mg/dL, Phosphorus 2.2 mg/dL, Intact PTH 95 pg/mLPrimary hyperparathyroidism
  • Calcium 12.8 mg/dL, Phosphorus 2.4 mg/dL, Intact PTH 5 pg/mLHypercalcemia of malignancy
  • Calcium 7.6 mg/dL, Phosphorus 5.8 mg/dL, Intact PTH 150 pg/mLChronic kidney disease
  • Calcium 8.1 mg/dL, Phosphorus 2.1 mg/dL, Intact PTH 135 pg/mLVitamin D deficiency

Answer

Profile 1 matches Primary hyperparathyroidism, Profile 2 matches Hypercalcemia of malignancy, Profile 3 matches Chronic kidney disease, and Profile 4 matches Vitamin D deficiency.
Each laboratory profile distinctly reflects the underlying pathophysiology of a specific calcium disorder. Primary hyperparathyroidism is characterized by autonomous PTH secretion leading to high calcium and low phosphorus. In hypercalcemia of malignancy, calcium is elevated via alternative pathways (like PTHrP or bone metastases), which strongly suppresses endogenous PTH. Chronic kidney disease results in phosphate retention and impaired calcitriol synthesis, causing low calcium, high phosphorus, and high PTH. Vitamin D deficiency results in poor intestinal absorption of both calcium and phosphorus; the subsequent secondary hyperparathyroidism normalizes or attempts to normalize calcium but further lowers phosphorus via renal wasting.

Step-by-Step Solution

1
Analyze the first laboratory profile.
Identified hypercalcemia coupled with elevated intact PTH and hypophosphatemia.
This pattern points to a primary overproduction of parathyroid hormone, as physiological PTH should be suppressed by hypercalcemia.
2
Analyze the second laboratory profile.
Identified severe hypercalcemia with appropriately suppressed intact PTH.
The suppressed PTH indicates a non-parathyroid source of hypercalcemia. The concurrent low phosphorus suggests a PTH-receptor agonist is at work, classically PTHrP seen in malignancy.
3
Analyze the third laboratory profile.
Identified hypocalcemia and hyperphosphatemia with elevated PTH.
The combination of elevated phosphorus and low calcium despite high PTH points to end-organ unresponsiveness and impaired filtration, which is the hallmark of chronic kidney disease.
4
Analyze the fourth laboratory profile.
Identified hypocalcemia and hypophosphatemia with elevated PTH.
The dual deficiency of calcium and phosphorus stems from a primary lack of gastrointestinal absorption, pointing directly to vitamin D deficiency. The elevated PTH reflects a secondary response.

Key Concept

Interpreting calcium, phosphorus, and parathyroid hormone levels together to differentiate the underlying etiologies of calcium homeostasis disorders.
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Interpreting Laboratory Results

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