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Difficulty: MediumEndocrinology and Metabolism

Match the following clinical patient vignettes with their most likely corresponding calcium, phosphorus, and parathyroid hormone (PTH) laboratory profiles.

  • A 60-year-old woman with recurrent calcium oxalate nephrolithiasis and recently diagnosed osteopenia.High serum calcium, low serum phosphorus, inappropriately normal or high intact PTH, and high 2424-hour urine calcium.
  • A 55-year-old man with diabetic nephropathy and an estimated glomerular filtration rate of 15 mL/min/1.73 m215 \text{ mL/min}/1.73 \text{ m}^2.Low serum calcium, high serum phosphorus, and appropriately high intact PTH.
  • A 70-year-old man with a 50-pack-year smoking history, a central lung mass, lethargy, and severe constipation.High serum calcium, low serum phosphorus, and suppressed intact PTH.
  • A 45-year-old woman presenting with perioral numbness and carpopedal spasm three days after a total thyroidectomy.Low serum calcium, high serum phosphorus, and inappropriately low intact PTH.
  • A 28-year-old asymptomatic man incidentally found to have mild hypercalcemia; his father has a similar history of benign hypercalcemia.High serum calcium, normal serum phosphorus, inappropriately normal or high intact PTH, and very low 2424-hour urine calcium.

Answer

Primary hyperparathyroidism maps to high Ca, low PO4, high PTH, high urine Ca. CKD maps to low Ca, high PO4, high PTH. Malignancy maps to high Ca, low PO4, suppressed PTH. Post-surgical hypoparathyroidism maps to low Ca, high PO4, low PTH. Familial hypocalciuric hypercalcemia maps to high Ca, normal PO4, high PTH, low urine Ca.
Each vignette represents a distinct disruption of calcium homeostasis. Primary hyperparathyroidism features autonomous PTH secretion, raising calcium and lowering phosphorus, accompanied by hypercalciuria. Secondary hyperparathyroidism from CKD is driven by phosphate retention and absent 1,25-dihydroxyvitamin D, causing hypocalcemia and an appropriate rise in PTH. Humoral hypercalcemia of malignancy is mediated by PTHrP, which mimics PTH but suppresses endogenous intact PTH. Surgical hypoparathyroidism physically removes the source of PTH, lowering calcium and raising phosphorus. Familial hypocalciuric hypercalcemia alters the calcium-sensing receptor threshold, resulting in mild hypercalcemia, normal/high PTH, and extreme renal calcium conservation (hypocalciuria).

Step-by-Step Solution

1
Diagnose the underlying condition for each clinical vignette.
Left 1 is primary hyperparathyroidism. Left 2 is secondary hyperparathyroidism (CKD). Left 3 is humoral hypercalcemia of malignancy. Left 4 is acquired hypoparathyroidism. Left 5 is familial hypocalciuric hypercalcemia (FHH).
Identifying the clinical syndrome is the mandatory first step before attempting to predict the resulting laboratory profiles.
2
Identify the expected PTH response based on the primary pathology.
Primary HPTH, Secondary HPTH, and FHH feature elevated or inappropriately normal PTH. Post-surgical hypoparathyroidism features inappropriately low PTH. Malignancy features suppressed PTH.
The intact PTH level distinguishes primary parathyroid disorders from compensatory responses and ectopic mechanisms (PTHrP).
3
Use serum calcium and phosphorus to differentiate the remaining disorders.
PTH drives calcium up and phosphorus down. Thus, high PTH with low Ca and high PO4 indicates secondary HPTH (the kidneys cannot respond). High PTH with high Ca and low PO4 indicates primary HPTH.
Phosphate handling clearly separates primary parathyroid overactivity from secondary hyperparathyroidism due to renal failure.
4
Use 24-hour urine calcium to distinguish primary hyperparathyroidism from FHH.
Primary HPTH causes high urine calcium due to an immense filtered load. FHH causes very low urine calcium due to a mutated calcium-sensing receptor that maximizes renal calcium retention.
These two conditions have nearly identical serum profiles (hypercalcemia with unsuppressed PTH) and require urine calcium for differentiation.

Key Concept

Disorders of Calcium and Phosphorus Homeostasis
Estimated Time:2m 0s
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Topics

Endocrinology and Metabolism

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