Two days after successful parathyroidectomy for severe primary hyperparathyroidism, a patient develops perioral tingling, carpopedal spasm, and seizures. Calcium is 6.0 mg/dL, phosphate is 2.8 mg/dL (elevated), and alkaline phosphatase is markedly raised. Intravenous calcium infusion produces only transient correction requiring escalating doses. What is the mechanism?

• A Removal of an ectopic mediastinal adenoma causing recurrent laryngeal nerve oedema
• B Rapid remineralisation of demineralised skeleton precipitating profound hypocalcaemia and hypophosphataemia ✓
• C Permanent hypoparathyroidism from excision of all four glands mistaken for an adenoma
• D Citrate toxicity from perioperative blood transfusion chelating ionised calcium

Explanation

This is hungry bone syndrome: after prolonged high PTH drive is removed, osteoblasts aggressively take up calcium, magnesium, and phosphate, causing severe, refractory hypocalcaemia. The clue distinguishing it from simple surgical hypoparathyroidism is the LOW phosphate with very high alkaline phosphatase reflecting bone turnover; ordinary postoperative hypoparathyroidism raises phosphate because renal excretion falls. Treatment requires large-volume IV calcium plus magnesium and often active vitamin D analogues.

Reference: Williams Textbook of Endocrinology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.