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Hungry bone syndrome post hyperparathyoidism – review Feb 2013

THERAPY OF ENDOCRINE DISEASE: Hungry bone syndrome: still a challenge in the post-operative management of primary hyperparathyroidism: a systematic review of the literature

Eur J Endocrinol March 1, 2013 168 R45-R53
J E Witteveen1, j.e.witteveen at lumc.nl)
S van Thiel1,2,
J A Romijn1,3 and
N A T Hamdy1
1 Department of Endocrinology and Metabolic Diseases, Leiden University Medical Center, Leiden, The Netherlands
2 Department of Internal Medicine, Amphia Medical Center, Breda, The Netherlands and
3 Department of Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcaemia associated with hypophosphataemia and hypomagnesaemia, and is exacerbated by suppressed parathyroid hormone (PTH) levels, which follows parathyroidectomy in patients with severe primary hyperparathyroidism (PHPT) and preoperative high bone turnover. It is a relatively uncommon, but serious adverse effect of parathyroidectomy. We conducted a literature search of all available studies reporting a ‘hungry bone syndrome’ in patients who had a parathyroidectomy for PHPT, to identify patients at risk and address the pitfalls in their management. The severe hypocalcaemia is believed to be due to increased influx of calcium into bone, due to the sudden removal of the effect of high circulating levels of PTH on osteoclastic resorption, leading to a decrease in the activation frequency of new remodelling sites and to a decrease in remodelling space, although there is no good documentation for this. Various risk factors have been suggested for the development of HBS, including older age, weight/volume of the resected parathyroid glands, radiological evidence of bone disease and vitamin D deficiency. The syndrome is reported in 25–90% of patients with radiological evidence of hyperparathyroid bone disease vs only 0–6% of patients without skeletal involvement. There is insufficient data-based evidence on the best means to treat, minimise or prevent this severe complication of parathyroidectomy. Treatment is aimed at replenishing the severe calcium deficit by using high doses of calcium supplemented by high doses of active metabolites of vitamin D. Adequate correction of magnesium deficiency and normalisation of bone turnover are required for resolution of the hypocalcaemia which may last for a number of months after successful surgery. Preoperative treatment with bisphosphonates has been suggested to reduce post-operative hypocalcaemia, but there are to date no prospective studies addressing this issue.

Received 15 June 2012
Revised version received 1 November 2012
Accepted 13 November 2012
Made available online as an Accepted Preprint 14 November 2012
© 2013 European Society of Endocrinology

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