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Zorluk: OrtaEndocrinology and Metabolism

Match the following calcium and parathyroid hormone (PTH) laboratory profiles with their most likely underlying etiologies.

  • Serum calcium 11.211.2 mg/dL, intact PTH 8585 pg/mL (high), 24-hour urine calcium 350350 mg/day (high)Primary hyperparathyroidism
  • Serum calcium 12.512.5 mg/dL, intact PTH 88 pg/mL (low), elevated parathyroid hormone-related peptide (PTHrP)Humoral hypercalcemia of malignancy
  • Serum calcium 11.011.0 mg/dL, intact PTH 5555 pg/mL (upper normal), urine calcium/creatinine clearance ratio <0.01<0.01Familial hypocalciuric hypercalcemia
  • Serum calcium 8.28.2 mg/dL, intact PTH 120120 pg/mL (high), 25-hydroxyvitamin D 99 ng/mL (low)Secondary hyperparathyroidism due to vitamin D deficiency

Cevap

The correct matches are: Profile 1 pairs with Primary hyperparathyroidism; Profile 2 pairs with Humoral hypercalcemia of malignancy; Profile 3 pairs with Familial hypocalciuric hypercalcemia; and Profile 4 pairs with Secondary hyperparathyroidism due to vitamin D deficiency.
Correctly matching these profiles requires evaluating the integrity of the parathyroid axis. When calcium is elevated, PTH should normally be suppressed. If PTH is high or inappropriately normal, the process is PTH-dependent (e.g., primary hyperparathyroidism or FHH). FHH must be distinguished from primary hyperparathyroidism by finding profound hypocalciuria due to a mutated calcium-sensing receptor. If PTH is suppressed, the hypercalcemia is PTH-independent, and the presence of elevated PTHrP points directly to a malignant etiology. Conversely, low calcium should appropriately stimulate PTH secretion; a concurrent low 25-hydroxyvitamin D level identifies secondary hyperparathyroidism as the underlying cause.

Adım Adım Çözüm

1
Evaluate the first laboratory profile.
The profile shows hypercalcemia, an elevated PTH, and hypercalciuria.
An elevated PTH in the setting of hypercalcemia indicates that the parathyroid glands are functioning autonomously rather than responding to physiological feedback. The resulting high filtered load of calcium causes hypercalciuria, confirming primary hyperparathyroidism.
2
Evaluate the second laboratory profile.
The profile reveals hypercalcemia with suppressed PTH and elevated PTHrP.
The suppressed PTH demonstrates intact physiological negative feedback from the hypercalcemia. The presence of PTHrP indicates that an ectopic source (e.g., squamous cell carcinoma) is driving the hypercalcemia, confirming humoral hypercalcemia of malignancy.
3
Evaluate the third laboratory profile.
The profile demonstrates hypercalcemia, an inappropriately normal PTH, and profound hypocalciuria (calcium/creatinine clearance ratio <0.01).
This pattern mimics primary hyperparathyroidism but is distinguished by the very low urine calcium excretion. It confirms familial hypocalciuric hypercalcemia (FHH), which results from a defective calcium-sensing receptor.
4
Evaluate the fourth laboratory profile.
The profile displays low calcium, elevated PTH, and low 25-hydroxyvitamin D.
The low vitamin D level leads to decreased intestinal calcium absorption. The parathyroid glands respond appropriately to the resulting low serum calcium by secreting more PTH, confirming secondary hyperparathyroidism.

Anahtar Kavram

Differential diagnosis of calcium and parathyroid disorders based on the relationship between serum calcium, intact PTH, and urinary calcium excretion.
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Endocrinology and Metabolism

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