Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2017) 48 CB9 | DOI: 10.1530/endoabs.48.CB9

Pilgrim Hospital, Boston, Lincolnshire, UK.


Summary: A case of intermittent hypercalcemia with a suppressed parathyroid hormone (PTH) for nearly 3 years. It was found that high calcium specifically occurred in summer and each one lasted for about a month. Once calcium normalised the renal function also improved. Exact aetiology has not been found even after extensive investigations.

Case presentation: A 67-year-old gentleman first presented to the endocrine clinic in early 2014 with Hypercalcemia. Tests revealed hypercalcemia (adjusted calcium 2.76 mmol/l) with supressed PTH (0.7 pmol/l), and low vitamin D of 44 nmol/l. The working diagnosis was hypercalcemia with suppressed PTH. Bendroflumethazide was stopped and no other precipitants found. He also had mild anaemia and mild renal impairment (previously normal renal function). Calcium normalised with hydration.

Subsequent investigations showed negative myeloma screen. CT CAP in 02/2014 showed bilateral multiple areas of ground glass opacification. Chest physicians diagnosed it as possible sarcoidosis, however appearances resolved on follow up CT done on 08/2014.

Since early 2014 he had few more admissions in Aug 2014, Jul 2015 and Jul 2016; notably all these admissions were in summer and he presented with hypercalcaemia with suppressed PTH and acute kidney injury. In between these admissions, his calcium remained normal. In July 2016, he developed Complete heart block which has not resolved with correction of calcium and a pacemaker was inserted. Repeat CT CAP in 08/2016 did not show any features of malignancy or reveal any lung parenchymal disease or any features of sarcoidosis. More extensive investigations were performed including PTHrP, 1,25 vitamin D and serum ACE, all of which came back normal. He had recent admission in November 2016 with similar presentation. This time it was precipitated by a small dose of Cholecalciferol. It returned to normal with adequate hydration and iv bisphosphonate.

Questions to the panel:

i) The cause of Hypercalcemia, is it cyclical hypercalcemia?

ii) Are there any other investigations that need to be done?

iii) Is there any genetic cause?

iv) Is it sarcoidosis which is intermittently active? If it is the case, how do we diagnose?

Volume 48

Society for Endocrinology Endocrine Update 2017

Society for Endocrinology 

Browse other volumes

Article tools

My recent searches

No recent searches.

My recently viewed abstracts