Hungry Bones Syndrome

Hungry Bones Syndrome

Transient hypoparathyroidism after resecting significant amounts of parathyroid gland, which were secreting excess PTH—due to hyperplasia or an adenoma—resulting in high alkaline phosphatase and significant bone demineralisation, and rapid ‘rebound’ recalcification of bones after prolonged hypocalcemia; bone hunger is exacerbated by pre-existing renal dysfunction
Lab Increased calcitriol, markedly decreased Ca2+ (e.g., 1.5 mmol/L—US: 6 mg/dl or lower), decreased phosphorus, decreased magnesium, reactive increase in PTH—if there is residual secretion; the danger lies in attributing symptoms to acidosis, which may accompany and exacerbate the complex Management Vitamin 1,25(OH)D2

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hungry bones syndrome

Post-parathyroid surgery recalcification tetany Metabolism Transient hypoparathyroidism due to resection of significant portions of a hyperactive parathyroid gland; HBs follow high pre-operative PTH–due to excess PTH secretion as occurs in parathyroid hyperplasia and adenoma, high alk phos and extensive bone demineralization, resulting in a rapid 'rebound' recalcification of bones after prolonged hypocalcemia; bone hunger is exacerbated by a pre-existing compromise in renal function Radiology Mottled bone hypodensity Lab ↑ Calcitriol, ↓↓↓ Ca2+–eg, 1.5 mmol/L–US: 6 mg/dl or lower, ↓ phosphorus, ↓ magnesium, reactive ↑ in PTH–if there is residual secretion; the danger lies in attributing Sx to acidosis, which may accompany and exacerbate the complex Treatment Vitamin 1,25(OH)D₂