Abstract
A 21-year-old woman presented to hospital with abdominal pain and nausea. She had a history of Graves’ disease which had been effectively treated with carbimazole for 15 months. Investigations revealed a serum adjusted calcium level of 3.69 mmol/L with a suppressed parathyroid hormone, thyroid stimulating hormone <0.01 mu/L (0.2–5.0) and free T4 of 76.1 pmol/L (9-24). She was treated as a relapsed case of Graves’ disease and started on propylthiouracil. Calcium levels continued to increase over the next 3 days despite adequate fluid resuscitation. A decision was taken to administer intravenous bisphosphonate (pamidronate) which resulted in a lowering of calcium levels. She became mildly hypocalcaemic following treatment with pamidronate which was presumed secondary to low vitamin D and oral vitamin D replacement was commenced. This case was unique as this is to our knowledge the most significant hypercalcaemia observed in a patient with hyperthyroidism. All other causes of hypercalcaemia were excluded. The learning points were recognising hypercalcaemia as a complication of thyrotoxicosis and the risk of hypocalcaemia following bisphosphonate therapy with low vitamin D stores.
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2 articles.
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