The patient

A 50 year old woman is found to have hypercalcaemia on routine blood tests. Her corrected calcium concentration was 2.75 (reference range 2.10-2.60) mmol/l, and phosphate 0.7 mmol/l (0.7-1.4) mmol/l. She had no history of abdominal pain, constipation, renal calculi, fractures, or mood disturbances. She was euvolaemic with no signs of chronic renal disease. Routine laboratory tests—including full blood count, serum electrolytes, and renal and liver function—were normal.

As her hypercalcaemia was mild, she did not require immediate measures to correct this. Investigations to determine the cause of the hypercalcaemia were performed.

About 40-50% of serum calcium is bound to protein (mostly albumin), and the remaining calcium is free or ionised (the portion under hormonal regulation). Corrected calcium is calculated from total calcium and serum albumin and an accurate reflection of ionised calcium in an individual with a normal serum albumin and normal acid-base balance. Asymptomatic hypercalcaemia (based on corrected or ionised values) is nowadays a common diagnostic and management dilemma, with more patients undergoing routine blood tests for other purposes. However, not all cases require treatment.

Primary hyperparathyroidism and malignancy together account for 90% of all hypercalcaemic patients.1 Aetiology varies according to the clinical presentation; more indolent cases suggest hyperparathyroidism, and more rapidly developing cases suggest malignancy. About 20-30% of all patients with cancer develop hypercalcaemia at some time as a paraneoplastic phenomenon or as a result of bone metastases.2 Dehydration exacerbates underlying hypercalcaemia by reducing renal calcium excretion, and drugs such as thiazide diuretics4 and lithium may exacerbate the underlying hypercalcaemia of primary hyperparathyroidism. The box outlines other causes of hypercalcaemia.