Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2011) 25 P338

SFEBES2011 Poster Presentations Thyroid (43 abstracts)

A case of Graves’ disease associated with severe hypercalcaemia

Sarah Ali , Katie Wynne & Karim Meeran

Endocrine Unit, Imperial College Healthcare NHS Trust, London, UK.

A 25-year lady was referred by her GP with a six-month history of symptoms suggestive of thyrotoxicosis; weight loss, palpitations, heat intolerance and lethargy. She also complained of thirst, polyuria and nocturia. Examination findings included tachycardia, tremor and a moderately enlarged goitre.

In clinic, blood tests performed confirmed thyrotoxicosis: TSH<0.05 mU/l (NR 0.3–4.2 mU/l), free T3 >46.1 pmol/l (NR 2.5–5.7 pmol/l) and free T4 69.1 pmol/l (NR 9.0–26.0 pmol/l). Serum anti-TSH receptor antibody was positive (>30.0 u/ml; NR 0–0.4 u/ml). Interestingly, corrected calcium was significantly raised at 3.35 mmol/l (NR 2.15–2.60 mmol/l), phosphate was 1.50 mmol/l (NR 0.8–1.4 mmol/l) and parathyroid hormone was non-suppressed but low-normal: 2.1 pmol/l (NR 1.1–6.8 pmol/l). Alkaline phosphate was normal and other causes of hypercalcaemia were excluded.

She was admitted for treatment of the hypercalcaemia with aggressive intravenous fluids. Carbimazole 20 mg tds and propranolol 40 mg tds were concurrently started. She was discharged home once the corrected calcium fell to 2.79 mmol/l and was closely followed up in the outpatient setting.

Following aggressive treatment of the Graves’ disease, biochemical results were significantly better two weeks later, including resolution of the hypercalcaemia (TSH<0.05 mU/l, fT4 16.0 pmol/l, fT3 4.2 pmol/l, corrected Ca 2.14 mmol/l, phosphate 0.87 mmol/l, PTH 2.5 pmol/l). This severe hypercalcaemia was therefore attributed to thyrotoxicosis as opposed to primary hyperparathyroidism. Interestingly, this lady was seen in clinic two months later and due to five weeks of noncompliance with Carbimazole, she was once again thyrotoxic and hypercalcaemic.

Conclusions: Thyrotoxicosis is commonly associated with abnormalities in bone metabolism, however the resultant hypercalcaemia is usually mild and asymptomatic. If hypercalcaemia is severe and symptomatic, there is often an alternative cause. In support of severe hypercalcaemia due to thyrotoxicosis is the reversal of hypercalcaemia with treatment of the hyperthyroidism. This case is interesting as thyrotoxicosis with such marked hypercalcaemia is uncommon and a corrected calcium of 3.35 mmol/l appears to be one of the most significantly elevated levels reported.

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