We present a case of a 50 year old patient with sepsis and a significant and symptomatic hypercalcaemia of 3.38 mmol/l with a background of MS. The infection responded to treatment however the hypercalcaemia persisted despite appropriate measures. Further investigation showed a suppressed PTH, normal ACE level, electrophoresis and 25(OH) vitamin D level, but found her to be thyrotoxic with TSH suppressed at <0.01, free T4 37.2 nmol/l, free T3 212 nmol/l. She has no previous history of thyroid disease. Treatment of the thyrotoxicosis with PTU resulted in a state of euthyroidism and also led to the resolution of her hypercalcaemia.
Loss of bone mineral density is a common phenomenon in patients with hyperthyroidism however biochemical hypercalcaemia is uncommon and for the patient to be symptomatic even rarer. When it does present it can hinder the detection of hyperthyroidism.
In our case the symptoms of sepsis and hypercalcaemia meant that the clinical signs of thyrotoxicosis were overlooked. It is important to consider thyroid disease as a cause of hypercalcaemia in patients not responding to usual management. It appears in our case that the thyrotoxicosis, immobility from MS and sepsis induced dehydration combined to give her such a significantly raised calcium.