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Hungry Bone Syndrome (HBS)

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Parathyroid Gland Disorders

Abstract

Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcemia associated with hypophosphatemia and hypomagnesemia, and is exacerbated by suppressed parathyroid hormone (PTH) levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism (PHPT) and pre-operative high bone turnover. It is a relatively uncommon, but a serious adverse effect of parathyroidectomy. The hallmark of HBS is profound and persistent hypocalcemia that persists beyond 4 days post-operatively. Symptomatic patients or those with profound hypocalcemia less than 7.6 mg/dL will need emergent intravenous calcium treatment. There are no clear guidelines for the management of the HBS, but treatment is aimed at replenishing the severe calcium deficit and at restoring normal bone turnover with the use of high doses of calcium and active metabolites or analogues of vitamin D. Adequate correction of magnesium deficiency and normalization of bone turnover are required for resolution of the hypocalcemia, which may last for several months after successful surgery. Adequate pre-operative treatment with bisphosphonates may reduce the severity and duration of post-operative hypocalcemia. However, data are lacking to elucidate the long-term effects on bone mineral density if utilized in this patient population. In patients with PHPT and vitamin D deficiency, vitamin D supplementation merits consideration. Thus far, it appears that vitamin D supplementation will help to improve bone mineral density, bone resorption markers, and reduce PTH levels before parathyroidectomy without causing adverse effects.

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Sakr, M.F. (2022). Hungry Bone Syndrome (HBS). In: Parathyroid Gland Disorders. Springer, Cham. https://doi.org/10.1007/978-3-031-07418-9_11

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