Hungry bone syndrome (HBS) refers to the rapid, profound, and prolonged hypocalcemia associated with hypophosphatemia and hypomagnesemia 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. The severe hypocalcemia 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 remodeling sites and to a decrease in remodeling 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 to 90% of patients with radiological evidence of hyperparathyroid bone disease vs only 0 to 6% of patients without skeletal involvement. There is insufficient data-based evidence on the best means to treat, minimize 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. Preoperative treatment with bisphosphonates has been suggested to reduce postoperative hypocalcemia, but there are to date no prospective studies addressing this issue.

Keywords: Bisphosphonates, Hyperparathyroid bone disease, Osteoclastic resorption, Parathyroidectomy, Postoperative hypocalcemia.

How to cite this article: Kadam RV, Mukhi LS, Deshmukh AG, Bahuva VD. Hungry Bone Syndrome due to Primary Parathyroid Adenoma with Multiple Bone Fractures. MGM J Med Sci 2015;2(2):103-105.

Source of support: Nil

Conflict of interest: None