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Difficulty: MediumEndocrinology and Metabolism

Review the distinct patterns of serum calcium, phosphorus, and parathyroid hormone (PTH) abnormalities described below. Match each clinical and laboratory profile with its corresponding endocrine or metabolic disorder.

  • Calcium 11.2 mg/dL, Phosphorus 2.2 mg/dL, PTH 85 pg/mL (elevated). Patient has a history of recurrent calcium oxalate nephrolithiasis.Primary hyperparathyroidism
  • Calcium 13.5 mg/dL, Phosphorus 2.1 mg/dL, PTH <5 pg/mL (suppressed), PTHrP elevated. Patient has a central lung mass.Humoral hypercalcemia of malignancy
  • Calcium 7.1 mg/dL, Phosphorus 5.8 mg/dL, PTH 8 pg/mL (suppressed). Patient recently underwent a total thyroidectomy.Primary hypoparathyroidism
  • Calcium 8.2 mg/dL (low-normal), Phosphorus 2.4 mg/dL, PTH 120 pg/mL (elevated), 25-hydroxyvitamin D 8 ng/mL (low). Patient has bone pain and a history of gastric bypass.Severe vitamin D deficiency (osteomalacia)
  • Calcium 8.0 mg/dL, Phosphorus 6.5 mg/dL, PTH 350 pg/mL (markedly elevated), estimated GFR 12 mL/min/1.73 m². Patient has chronic fatigue and lower extremity edema.Secondary hyperparathyroidism due to chronic kidney disease

Answer

The clinical profiles map to primary hyperparathyroidism, humoral hypercalcemia of malignancy, primary hypoparathyroidism, vitamin D deficiency, and secondary hyperparathyroidism due to chronic kidney disease based on the physiologic interplay of calcium, phosphorus, and parathyroid hormone.
Correct matching requires identifying the primary driver of the electrolyte abnormality based on normal physiological feedback loops. In primary hyperparathyroidism and malignancy, calcium is elevated; they are differentiated by endogenous PTH levels (high/inappropriate in primary hyperparathyroidism, suppressed in malignancy). In primary hypoparathyroidism, vitamin D deficiency, and chronic kidney disease, calcium is low or low-normal. They are differentiated by PTH and phosphorus: low PTH indicates primary hypoparathyroidism; high PTH with low phosphorus points to vitamin D deficiency; and high PTH with high phosphorus points to chronic kidney disease.

Step-by-Step Solution

1
Evaluate the first profile (high calcium, low phosphorus, high PTH).
Matches Primary hyperparathyroidism.
An inappropriately high PTH in the setting of hypercalcemia indicates autonomous secretion, typical of a parathyroid adenoma.
2
Evaluate the second profile (high calcium, low phosphorus, suppressed PTH, elevated PTHrP).
Matches Humoral hypercalcemia of malignancy.
The central lung mass secretes PTH-related peptide, which raises calcium and lowers phosphorus, successfully suppressing normal parathyroid gland PTH output via negative feedback.
3
Evaluate the third profile (low calcium, high phosphorus, low PTH).
Matches Primary hypoparathyroidism.
Post-thyroidectomy status suggests iatrogenic gland damage, leading to an absolute deficiency of PTH and consequent inability to reabsorb calcium or excrete phosphorus.
4
Evaluate the fourth profile (low-normal calcium, low phosphorus, high PTH, low vitamin D).
Matches Severe vitamin D deficiency (osteomalacia).
Gastric bypass causes malabsorption of fat-soluble vitamin D. The resulting hypocalcemia stimulates the parathyroid glands to secrete PTH, which corrects the calcium slightly but wastes phosphorus in the urine.
5
Evaluate the fifth profile (low calcium, high phosphorus, very high PTH, low GFR).
Matches Secondary hyperparathyroidism due to chronic kidney disease.
Failing kidneys cannot excrete phosphorus or activate vitamin D. Retained phosphorus and low active vitamin D drive persistent hypocalcemia, leading to massive compensatory PTH release.

Key Concept

Pathophysiology and laboratory interpretation of calcium and phosphorus metabolic disorders
Estimated Time:2m 0s
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Topics

Endocrinology and Metabolism

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