Endocrine Abstracts

Hypercalcemia in hyperthyroidism is usually asymptomatic, and related to a concurrent primary hyperparathyroidism. In this report, we describe a case of symptomatic hypercalcemia secondary to Graves’ disease alone.

Case report: A 24-year-old Filipino female presented to the emergency department with generalized weakness, vomiting and abdominal pain. No other symptoms were noted. She was otherwise previously healthy. Family history was unremarkable. During physical exam, she was noted to have a non tender palpable thyroid gland without bruit. Her ECG showed sinus tachycardia. The complete blood count and electrolytes were normal however, ionized calcium was high at 1.6 mmol/l (NV 1–1.3). Renal function was normal. Hydration with saline and Furosemide 20 mg once daily was started though calcium levels remained elevated. Other causes of hypercalcemia were excluded as PTH was appropriate suppressed (8.8 ng/l; NV 14–72), vitamin D was also suppressed (15.29 nmol/LNV: >30). CT scan of chest and abdomen and bone scan did not point to any underlying malignancy nor metabolic bone disease. Medication history was also unremarkable. She was hyperthyroid with a suppressed thyroid stimulating hormone level of 0.004 pmol/l (NV:0.55–4.78), free T3 of >20 pmol/l (NV:2.3–4.2), free T4 of 8.4 pmol/l (NV:0.89–1.76). Thyroid receptor antibody levels were raised at 41.07 (NV:<1 kU/l) supporting the diagnosis of Graves’disease. She was started on propylthiouracil 50 mg four times daily, along with propranolol 40 mg three times daily. She was subsequently seen after two weeks with normal repeat calcium level and thyroid function test.

Conclusion: This report aims to highlight that thyroid disease should always be considered as a cause of hypercalcemia. It should be distinguished from concomitant primary hyperparathyroidism. The definitive treatment for the hypercalcemia is correction of thyroid function.