Category: Calcium/Bone Disorders

Monitor: 19


Friday, Apr 26
12:00 PM – 12:30 PM

Objective :

Rickets is rarely associated with progression to irreversible tertiary hyperparathyroidism (hPTH). Parathyroidectomy (PTHx) effectively treats this complication, but profound postoperative hypocalcemia (hCa) necessitates careful management. In the high turnover state associated with hPTH, PTH increases bone formation and resorption with a net efflux of Ca from bone to maintain serum Ca. The reductions in parathyroid hormone (PTH) and subsequent reduction in PTH-mediated renal 1,25-dihydroxycholecalciferol (1,25(OH)2D) production leads to a drive for calcium (Ca) into bone, increased Ca excretion from the kidneys and decreased intestinal Ca absorption. This imbalance results in a net increase in bone uptake of Ca, phosphorus (P) and magnesium (Mg) with a resulting fall in serum levels; also known as Hungry Bone Syndrome (HBS). HBS is more often seen in those who have known bone disease due to chronic increase in bone resorption from high levels of PTH, either primarily from parathyroid hyperactivity or secondarily from chronic kidney disease (CKD). We present a case of a HBS rooted from a deficit in the conversion from 25-dihydroxycholecalciferol (25(OH)2D) to (1,25(OH)2D).

Methods : n/a

Results :

Our patient is a 54-year-old man with history of congenital rickets with subsequent hPTH, type 2 diabetes mellitus, hypertension, hyperlipidemia, and CKD3. On 9/24/18 he underwent 3 gland PTHx for hPTH. He was discharged on postoperative day two with adequate Ca supplementation.

He returned on 10/13/2018 with confusion and fatigue. Labs showed Ca of 7.2, albumin 3.2, P 1.4, Mg 1.6, and potassium 4.2. Despite receiving replacement doses of Ca, Mg and P, his Ca remained around 7.1. Endocrinology was consulted and suspicions arose that he had HBS. He was started on Calcitriol 0.25mcg daily, Ca-Carbonate 500mg 4 times a day, and Mg-Oxide 800mg daily. 

Discussion : HBS refers to the rapid, profound, and prolonged hCa associated with low P and Mg, and is exacerbated by suppressed PTH levels following PTHx. It is relatively uncommon, but a serious adverse effect of PTHx. 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. There is insufficient data-based evidence on the best means to treat, minimise or prevent this severe complication of PTHx. Treatment is aimed at replenishing the severe Ca deficit by using high doses of Ca and vitamin D supplementation. Adequate correction of Mg deficiency and normalisation of bone turnover are required for resolution of the hCa which may last for a number of months after successful surgery.

Conclusion : n/a


Nicolas A. Mungo

Endocrinology Fellow
The University of Arizona
Oro Valley, Arizona


Leopoldo M. Cobos

Endocrinology Fellow
The University of Arizona


Juan Galvez

Endocrinologist, Associate Program Directory, Endocrinology, Diabetes and Metabolism Fellowship
The University of Arizona


Craig Stump