SFEEU2023 Society for Endocrinology Clinical Update 2023 Workshop F: Disorders of the parathyroid glands, calcium metabolism and bone (12 abstracts)
Department of Diabetes & Endocrinology, Northwick Park Hospital, London Northwest University Healthcare NHS Trust, London, United Kingdom
Introduction: Hypercalcaemia accounts for 0.6% of all acute medical admissions1, with primary hyperparathyroidism and malignancy-associated hypercalcaemia contributing to 90% of these cases.
Case Presentation: A 67-year-old female was initially seen in neurology clinic with a 3-year history of subtle word-finding difficulties, episodic confusion, and balance problems. On further probing, she reported constipation, polyuria and polydipsia, but had no other systemic symptoms. She had a past medical history of hypertension and was on regular Ramipril, Indapamide and calcium supplements. She had no significant family history. Following the clinic appointment, routine blood tests carried out showed elevated calcium levels of 3.13mmol/l and a normal HBA1C. Given findings of symptomatic hypercalcaemia, she was admitted to hospital and commenced on intravenous fluids (0.9% sodium chloride). Her Indapamide and calcium supplements were stopped. Investigations were carried out to determine the cause of her hypercalcaemia; phosphate levels were low (0.72mmol/l), parathyroid hormone (PTH) levels were raised (13.6 pmol/l) and Vitamin D was replete (140nmol/l). Renal function, alkaline phosphatase, magnesium, TSH, myeloma screen and serum ACE levels were normal. Her hypercalcaemia improved to below 2.8mmol/l with fluids and she was discharged from hospital with endocrine follow-up. In endocrine clinic, repeat blood tests showed an elevated calcium level greater than 2.85mmol/l and a non-suppressed PTH, with some ongoing symptoms. A 24-hour urinary calcium: creatinine clearance ratio was calculated at 0.02, confirming the diagnosis of primary hyperparathyroidism. Investigations were carried out to assess for end-organ damage; a renal tract ultrasound showed no evidence of calculi or nephrocalcinosis, but a DEXA scan revealed osteopenia of the spine. A thyroid ultrasound showed a probable right superior parathyroid adenoma which was in concordance with the Technetium (99mTc) Sestamibi (MIBI) scan. After further discussion with the patient, she was referred for consideration of a parathyroidectomy.
Conclusion: A systematic approach is key in the management of hypercalcaemia. Once primary hyperparathyroidism is confirmed, a clear explanation of the long-term consequences of excess PTH should be discussed with the patient with consideration of conservative and surgical management options. Further investigations should be carried out to assess for end-organ damage and to localise the source of elevated PTH, if surgical intervention is an option.
Reference: 1. Turner, J.J.O. (2017) Hypercalcaemia presentation and management, Clinical Medicine. Royal College of Physicians,17(3), pp.270273. doi:10.7861/CLINMEDICINE.17-3-270.