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Biochemistry · Vitamins and minerals: hungry bone syndrome
Sample itemThree days after parathyroidectomy for long-standing primary hyperparathyroidism with severe bone disease, a patient has perioral tingling and carpopedal spasm. Serum calcium is 6.8 mg/dL with low phosphate and magnesium, and PTH is within the normal range. What is the mechanism?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
D. Rapid deposition of mineral into demineralised bone
After removal of the adenoma, PTH-driven resorption stops while the depleted skeleton avidly takes up calcium, phosphate and magnesium. Calcium may stay low for weeks and needs large supplements with calcitriol. A normal PTH with low phosphate separates it from hypoparathyroidism, where phosphate is high.
Option by option
A. Resistance of the intestine to vitamin D
Intestinal vitamin D resistance does not follow parathyroid surgery.
B. Excess calcitonin from C cells
Calcitonin excess does not cause clinically significant hypocalcaemia.
C. Autoimmune destruction of the remaining parathyroids
Loss of parathyroid function would give a low PTH and a high phosphate.
D. Rapid deposition of mineral into demineralised bone (correct)
Correct. Avid skeletal uptake of mineral lowers calcium, phosphate and magnesium together, with preserved PTH.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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