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Endocrine Abstracts (2025) 109 CC8 | DOI: 10.1530/endoabs.109.CC8

SFEBES2025 Featured Clinical Case Posters Section (10 abstracts)

Severe refractory hypocalcaemia in metastatic breast cancer in patient with concurrent primary hypoparathyroidism

Wint Yupar , Beata Brown & Jana Bujanova


University Hospital Southampton, Southampton, United Kingdom


68y female with a history of autoimmune hypoparathyroidism and metastatic breast cancer with liver, lung and breast metastases developed severe refractory hypocalcaemia twice during introduction of different antitumour therapies for her metastatic disease in context of mixed type bone metastases and very stable calcium control on Alfacalcidol 1 mg and Adcal D3 (1500/400) once daily. She was diagnosed with breast cancer in 2015 and treated with wide local excission, adjuvant radiotherapy, tamoxifen and anastrozole. In 2020, developed predominantly sclerotic bone metastases. One month after commencing Fulvestrant in combination with Abemaciclib, her calcium dipped to 1.42 mmol/l (2.2-2.6) presumably due to high volume of sclerotic breast metastases. Hypocalcaemia responded to intavenous calcium, increase in oral calcium and alfacalcidol to 3 mg od for several months. In March 2024 there was progression in lytic metastases associated with significant ALP rise but stable calcium between 2.33- 2.53 mmol/l on Alfacalcidol 1 mg od and Adcal D3 1 tbl od. Two weeks after commencing Paclitaxel, she was admitted with symptomatic hypocalcemia of 1.45 mmol/l requiring prolonged iv calcium infusions, doubling in alfacalcidol, Adcal dose and eventually conversion to more potent calcitriol 2 mg am and 1 mg pm. There was no concurrent administration of biphoshonates or denosumab. Magnesium was mildly reduced at 0.61 mmol/l (0.7-1) and corrected intravenously.

Discussion: Breast cancer bone metastases are typically osteolytic or mixed type. Introduction of antitumour therapies can cause rapid shift in bone metabolism from osteolytic to osteoblastic, causing significant calcium absorption into the bone. This can cause severe hypocalcemia similar to ‘hungry bone syndrome’. This effect can be profound and prolonged in patients with concurrent hypoparathyroidism unable to mount PTH response and where calcium and activated vitamin D doses are not adjusted in anticipation of this effect. Careful calcium monitoring throughout the treatment is recommended.

Volume 109

Society for Endocrinology BES 2025

Harrogate, UK
10 Mar 2025 - 12 Mar 2025

Society for Endocrinology 

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