Hungry Bone Syndrome Associated with Transient Hypoparathyroidism

Hypoparathyroidism 

It is a state of inadequate parathyroid hormone (PTH). It results from defective synthesis or secretion of PTH, end organ resistance, or inappropriate regulations. Hypoparathyroidism may be transient, genetically inherited or acquired. Transient usually occurs during neonatal period or secondary to medication. The ionized calcium concentration, in extracellular fluid (ECF), falls below the reference range, where at birth parathyroid gland have a limited ability to respond to decrease in serum calcium.

We present an infant with transient hypoparathyroidism who developed the severe hungry bone syndrome. Such an association is highlighted.

case presentation

A full term, 50 day-old Saudi male boy, presented to the emergency department with afebrile tonic-clonic seizure lasting for several minutes and aborted by rectal diazepam. Pregnancy and neonatal history were unremarkable, in particular, the mother was not on any medication. No family history of seizure disorder. He was appropriate for age and there were no dysmorphic features.

The patient was initially managed with intravenous calcium infusion, then later with oral calcium (50mg/kg/day) in four divided doses and calitriol (1,25 dihydroxycholecalciferol ). Three weeks later re-admitted again with afebrile seizure, serum calcium was 1.2 mmol/L (normal 2.2 - 2.5). He requires high dose of calcium (200mg/kg/day), in addition to calcitriol. No further seizure, and was discharged after one week of hospitalization on calcium and calcitriol, with serum calcium of 2.3 mmol/L, subsequently, he was followed in the endocrine clinic, and within three months his medication was gradually withdrawn. He continued to be well off therapy with serum calcium ranging between 2.2 - 2.4 mmol/ L, and serum concentration of PTH 3.2 pmol/L (normal 1.6 - 6.9). At time of reporting the case, he is currently 5 years of age with normal bone profile and PTH serum concentration. He is neurodevelopmentally appropriate for age.

The diagnosis of transient hypoparathyroidism, in our patient, was established on basis of low PTH and calcium, with high phosphate and normal alkaline phosphatase, which returned to normal after three months of therapy. The infant did not receive any medications such as amphotericin B nor had hypo or hypermagnesia.

Hungry bone syndrome is a well known entity associated with treatment of hypocalcemia. Continuous and frequent serum calcium monitoring is mandatory to avoid the two extreme complications, hypo, and hypercalcemia.

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