Hungry bone syndrome

Hungry bone syndrome presents as severe, prolonged hypocalcemia following parathyroidectomy for primary or secondary hyperparathyroidism, driven by the abrupt withdrawal of elevated PTH and accelerated skeletal remineralization. Definitive clinical management requires aggressive dual-route calcium repletion, combining continuous intravenous calcium gluconate for acute symptomatic crisis with high-dose oral elemental calcium up to 6 to 12 grams daily. High-dose calcitriol at 0.5 to 1.0 micrograms twice daily is critical to maximize active intestinal calcium transport. Concomitant correction of hypomagnesemia is mandatory, as magnesium deficiency impairs residual parathyroid function and induces calcitriol resistance. Titration requires frequent biochemical monitoring, with gradual weaning extending over weeks to months as bone turnover normalizes.