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Endocrine Abstracts (2022) 86 P143 | DOI: 10.1530/endoabs.86.P143

SFEBES2022 Poster Presentations Thyroid (41 abstracts)

A delayed diagnosis of Graves’ disease in a patent with severe hyperthyroidism-associated hypercalcaemia

Adil Ramzan , Satyanarayana V Sagi & Samson O Oyibo


Peterborough City Hospital, Peterborough, United Kingdom


Introduction: Mild hypercalcaemia can occur in patients with Graves’ disease. Postulated mechanisms include increased bone resorption and mobilisation of calcium from the bones in response to increased interleukin-6 and catecholamine levels. The coexistence of primary hyperparathyroidism and Graves’ disease is rare. Hypercalcaemia with suppressed or unsuppressed parathyroid hormone levels should prompt a search for non-parathyroid or parathyroid causes, respectively.

Case: A 71-year-old man presented with a history of vomiting and confusion for ten days, and weight loss of 24 kg over ten months. His medical history included ischaemic heart disease and type 2 diabetes. His usual medications included metformin, aspirin, alogliptin, ramipril, simvastatin and lansoprazole. He was a non-smoker. Examination revealed dehydration and mild confusion.

Investigations and management: His serum calcium was 3.19 mmol/l with an unsuppressed (normal) parathyroid hormone level of 4.1 pmo/l. Full blood count, serum electrophoresis, phosphate, renal and kidney function were normal. Urinalysis ruled out hypocalciuric hypercalcaemia. Chest x-ray and electrocardiogram were normal. Total body imaging ruled out underlying neoplasia. After rehydration, the patient was discharged from hospital. Parathyroid imaging (ultrasound, sestamibi, 4D-CT) and bone density scan were normal. However, he was readmitted three weeks later with a serum calcium of 3.16 mmol/l. Subsequent tests revealed a serum thyroid stimulating hormone of 0.01 mU/l, free thyroxine of 35.7 pmo/l, free triiodothyronine of 11.3 pmo/l, and raised thyroid receptor antibodies (TRAb), indicating Graves’ disease. He was started on Carbimazole 20 mg daily for the hyperthyroidism. His calcium levels returned to normal once his thyroid function was under control.

Conclusions: This patient had hyperthyroidism-associated hypercalcaemia. The diagnosis of Graves’ disease was delayed during the search for other causes of severe hypercalcaemia. This case emphasises the importance of thorough history taking and remembering hyperthyroidism as a cause of hypercalcaemia.

Volume 86

Society for Endocrinology BES 2022

Harrogate, United Kingdom
14 Nov 2022 - 16 Nov 2022

Society for Endocrinology 

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