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Orthopaedics · Metabolic bone disease: hungry bone syndrome
Sample itemA 45-year-old with severe primary hyperparathyroidism and brown tumours has a parathyroidectomy. Three days later he has perioral tingling and carpopedal spasm. Serum calcium and phosphate are both low, with PTH not suppressed. What is the mechanism?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Rapid uptake of calcium and phosphate by remineralising bone
Hungry bone syndrome follows parathyroidectomy when the fall in PTH switches off resorption but formation continues, and bone avidly takes up calcium, phosphate and magnesium. It is more likely with high pre-operative alkaline phosphatase and bone disease. Treatment is high-dose calcium and calcitriol, with magnesium replacement.
Option by option
A. Rapid uptake of calcium and phosphate by remineralising bone (correct)
Correct. Remineralising bone takes up calcium and phosphate, with low levels of both and a PTH that is not low.
B. Permanent hypoparathyroidism from removal of all glands
After complete gland removal the calcium is low but phosphate is high, and PTH is low or undetectable.
C. End-organ resistance to PTH
End-organ resistance, as in pseudohypoparathyroidism, causes low calcium with high phosphate and high PTH.
D. Vitamin D toxicity
Vitamin D toxicity raises calcium and phosphate rather than lowering them.
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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