An unusual case of severe and symptomatic hypercalcaemia in the context of thyrotoxicosis
Dr Abrar Gundroo, Professor Karim Meeran
A 27-year-old woman presented to our Endocrinology clinic with a six month history of thyrotoxic symptoms including weight loss of two stone, palpitations, tremors, fatigue, and sweating. Over the last six weeks she also described increasing polydipsia and polyuria, and persistent nausea and vomiting. On examination she was tremulous and tachycardic with signs of dehydration and a diffusely enlarged thyroid gland.
Thyroid function tests on admission revealed free T4 69.1 pmol/L (Normal Range 9.0–25.0 pmol/L), free T3 46.1 pmol/L (NR 0.3-4.2 pmol/L) and TSH <0.05 mU/L (NR 0.3-4.2 mU/L). Bone profile revealed a pronounced hypercalcaemia with adjusted calcium 3.34 mmol/L (NR 2.15–2.60 mmol/L), phosphate 1.50 mmol/L (NR 0.8–1.4 mmol/L) and an unsuppressed parathyroid hormone level of 2.1 pmol/L (NR 1.1-6.8 pmol/L). A positive TSH receptor antibody test confirmed Graves’ Disease and investigations to determine an alternative cause of her hypercalcaemia were all negative.
She was treated aggressively with high dose carbimazole, propanolol and intravenous fluids. She responded remarkably well to this, as investigations one week later showed normalised thyroid function (free T4 16.0 pmol/L, free T3 4.2 pmol/L), normalised adjusted calcium (2.10 mmol/L), and normal parathyroid hormone (2.5 pmol/L). Four months later she re-presented with thyrotoxicosis and severe hypercalcaemia following non-compliance with treatment, with free T4 69.8 pmol/L, free T3 46.1 pmol/L and adjusted calcium of 3.24 mmol/L. Once again this responded well to fluids and anti-thyroid treatment. Six months on, her thyroid function, calcium and parathyroid hormone levels were normal.
Hypercalcaemia in hyperthyroidism is usually mild and asymptomatic in the absence of concomitant pathology. Our case demonstrates two unusual findings; firstly a severe and symptomatic hypercalcaemia associated with thyrotoxicosis, which is responsive to fluids and anti-thyroid treatment. The hypercalcaemia is the most significant we have observed in this context. Secondly, the severe hypercalcaemia is associated with unsuppressed parathyroid hormone levels, in the absence of demonstrable parathyroid disease. The absence of parathyroid disease is supported by the reversal of hypercalcaemia following correction of hyperthyroidism and rehydration, and a normal calcium and parathyroid hormone level at six month follow-up. Our case would suggest that a diagnosis of primary hyperparathyroidism should not be made in the context of thyrotoxicosis.