Hypercalcaemia can be caused by many disorders, but is most commonly due to
primary hyperparathyroidism in outpatients, and to malignant disease in hospital inpatients. When mild (less than 3 mmol/L) it does not cause symptoms, but can have long term effects such as
renal calculi. It is important that the aetiology of the hypercalcaemia be established, as it can reflect serious disease. In most patients the correct diagnosis can be suspected from clinical history and examination, and confirmed by laboratory tests and x-rays. The most difficult diagnostic problem is the patient with negative clinical findings, mild hypercalcaemia and mild renal impairment, when the
parathyroid hormone level is normal or slightly elevated. When hypercalcaemia is severe (greater than 3.5 mmol/L), it can cause
vomiting,
polyuria,
dehydration and renal impairment, and is then an important therapeutic problem.
Therapy includes treatment of the cause, such as
radiotherapy for malignant disease or surgery for
primary hyperparathyroidism. In addition, it is usually necessary to treat the hypercalcaemia itself, and the initial step is always
rehydration. If the plasma
calcium concentration remains high,
drug treatment must be added, the most effective and reliable agent being intravenous
mithramycin.
Aminohydroxypropylidene diphosphonate (APD), though less studied, may be equally useful in this situation.
Glucocorticoids are not always effective, and
phosphate may cause renal damage, particularly when given intravenously. For long term treatment of malignant hypercalcaemia, oral
glucocorticoids and
phosphate are often effective, and can be given in combination. When
primary hyperparathyroidism cannot be corrected surgically, the hypercalcaemia (and
hypercalciuria) are probably best treated with a low
calcium diet and
cellulose phosphate, a regimen also effective for the hypercalcaemia of
sarcoidosis.