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Endocrine Abstracts (2017) 48 WF4 | DOI: 10.1530/endoabs.48.WF4

Ninewells Hospital & Medical School, Dundee, UK.


A previously well 50-year-old female was admitted to the acute medical unit with a 4-month history of fatigue, anorexia, polyuria, polydipsia and arthralgia. She was found to be hypercalcaemic with a corrected calcium of 3.84 mmol/l and, unexpectedly, an extremely elevated parathyroid hormone reported at >200 pmol/l. Other results included an elevated alkaline phosphatase, hypophosphataemia and normal renal function. Treatment with intravenous 0.9% sodium chloride and pamidronate resulted in amelioration of the patient’s symptoms. Her calcium improved only marginally, and she required ongoing intravenous rehydration to maintain a calcium level below 3 mmol/l. Ultrasonography of the neck and sestamibi scanning showed a right superior parathyroid mass. She was referred to an endocrine surgeon who went on to perform a parathyroidectomy and partial thyroidectomy. The clinical suspicion of parathyroid carcinoma was confirmed histopathologically. The patient’s hypercalcaemia resolved immediately and PTH returned to normal. She was subsequently discharged on oral vitamin D supplementation. Approximately 2 weeks following discharge, the patient began experiencing widespread muscle cramps and paraesthesia. Corrected calcium was 1.78 mmol/l and PTH was elevated at 40 pmol/l indicative of secondary hyperparathyroidism and ‘hungry bone syndrome’. She was treated with intravenous calcium infusion followed by oral calcium supplementation and high-dose alfacalcidol. This case reminds us that primary hyperparathyroidism is not always a benign condition and can rarely be due to parathyroid carcinoma. It also highlights the challenges of managing hypercalcaemia when the PTH is substantially elevated, the importance of hungry bone syndrome, and the necessity of liaison with our surgical colleagues in such cases.

Volume 48

Society for Endocrinology Endocrine Update 2017

Society for Endocrinology 

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