Hungry bone syndrome after parathyroidectomy for primary hyperthyroidism

Parathyroidectomy is the treatment of choice in patients with primary hyperparathyroidism (PHPT). This disease affects calcium metabolism at the level of bone tissue and renal tubules, resulting in hypercalcaemia, often asymptomatic, associated with hypophosphataemia and hypomagnesaemia. Sudden suppression of parathyroid hormone (PTH), caused by successful parathyroidectomy, in patients with preoperative high levels of PTH and hypercalcaemia from enhanced bone turnover, may induce severe postoperative hypocalcaemia that may lead to symptoms of tetany. This relatively uncommon condition is known as “hungry bone syndrome” (HBS), because it is believed to be due mainly to enhanced bone formation. Several risk factors have been advocated for HBS, and the syndrome is reported to be more likely to rise in subjects with severe preoperative bone disease. Other modifiable risk factors are preoperative vitamin D deficiency and high PTH and calcium levels. Treatment of HBS is basically the administration of high amounts of calcium immediately after the onset of postoperative hypocalcaemia. Supplements of active metabolites of vitamin D, as well as magnesium in depleted subjects are complementary in supporting bone remineralization. Oral supplementation may be requested for months after parathyroidectomy. Prevention is poorly documented, but it is reasonable to propose the correction of vitamin D deficit and the use of bisphosphonates aimed to lower PTH levels and bone resorption before parathyroidectomy.