Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2022) 81 P565 | DOI: 10.1530/endoabs.81.P565

ECE2022 Poster Presentations Calcium and Bone (68 abstracts)

A case of severe hypercalcaemia secondary to primary hyperparathyroidism responding to steroids

Susan Mathew 1 , Tracey Ellis 1 & Edward Jude 1,2


1Tameside and Glossop Integrated Care NHS Foundation Trust, United Kingdom; 2The University of Manchester, Manchester United Kingdom


Case History: A 57 year old male, who was known to have primary hyperparathyroidism was admitted to hospital due to hypercalcaemia on routine blood tests (adjusted S. calcium- 3.44 mmol/l.) He had no symptoms due to hypercalcaemia. This was his 5th admission since the diagnosis 18 months ago, each admission requiring treatment with IV fluids and IV bisphosphonates. SESTAMIBI and ultrasound scans of the thyroid and parathyroids had previously localised a likely right inferior parathyroid adenoma. Myeloma screen was negative. His past medical history included schizophrenia, vitamin D deficiency and psoriasis.

Treatment: He was initially treated with intravenous fluids, zolendronic acid and cinacalcet. Due to persistent hypercalcaemia, the dose of cinacalcet was increased to 60 mg TDS and intravenous calcitonin was added on. However, adjusted calcium remained around 3.4 mmol/l. He was hence re-referred to ENT surgeons for urgent parathyroidectomy. Unfortunately, he contracted COVID, which delayed the surgery. At this point, he was symptomatic with confusion, agitation, nausea, dehydration and abdominal cramps. He had repeat IV zolendronate 4 weeks from the previous dose and was also prescribed IV hydrocortisone 100 mg IV QDS 6 weeks into the hospital stay. The corrected calcium level reduced from 4.2 mmol/l to 2.2 mmol/l within a week. With the resolution of hypercalcaemia, his confusion resolved. He was switched to oral prednisolone 40 mg OD, which was slowly weaned down. His adjusted calcium levels started rising again shortly after the prednisolone was weaned. Three weeks later he had parathyroidectomy. Following this, his PTH level normalised from a peak pre-operative level of 660 pg/ml to 22 pg/ml post operatively. Two days following parathyroidectomy, he became hypocalcaemic with adjusted serum calcium of 1.92 mmol/l. He was discharged on 3000 mg of calcium carbonate and 1600 units of vitamin D3 daily. He was asymptomatic on follow-up.

Follow-up: The histopathology was suggestive of parathyroid carcinoma. He remains under endocrine and ENT follow-up.

Discussion: Parathyroid carcinoma should be suspected in cases with significantly raised PTH and resistant hypercalcaemia. Emergency parathyroidectomy should be considered in severe cases of hyperparathyroidism unresponsive to medical management. A trial of steroids may be useful as an adjunct in cases of severe resistant hypercalcaemia due to primary hyperparathyroidism, but remains an exception rather than the rule. The mechanism of action remains unknown. Potentiation of the action of calcitonin by upregulation of calcitonin receptors on osteoclast by steroids may be a plausible explanation.

Volume 81

European Congress of Endocrinology 2022

Milan, Italy
21 May 2022 - 24 May 2022

European Society of Endocrinology 

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