Primary hyperparathyroidism and
malignancy are responsible for greater than 90% of all cases of
hypercalcemia. Compared with the
hypercalcemia of
malignancy,
hyperparathyroidism tends to be associated with lower serum
calcium levels (< 12 mg/dL) and a longer duration of
hypercalcemia (more than 6 months). The hypercalcemic symptoms are usually fewer and subtle.
Hyperparathyroidism tends to cause
kidney calculi, hyperchloremic
metabolic acidosis, and the characteristics of
metabolic bone disease osteitis fibrosa cystica, but no
anemia. In contrast,
hypercalcemia of
malignancy is typically rapid in onset, with higher serum
calcium levels, and more severe symptoms. Patients so affected show marked
anemia, but they never have
kidney calculi or
metabolic acidosis.
Parathyroid hormone assay is the most useful test for differentiating
hyperparathyroidism from
malignancy and other causes of
hypercalcemia. In
hyperparathyroidism, serum
parathyroid hormone levels will be elevated. In other cases, the high serum
calcium concentration usually results in suppression of
parathyroid hormone. Treatment of
hypercalcemia should be started with hydration.
Loop diuretics may be required in individuals with
renal insufficiency or
heart failure to prevent fluid overload.
Calcitonin is administered for the immediate short-term management of severe symptomatic
hypercalcemia. For long-term control of severe or symptomatic
hypercalcemia, the addition of biphosphonate is typically required. Among intravenous
bisphosphonates,
zoledronic acid or
pamidronate are the agents of choice.
Glucocorticoids are effective in
hypercalcemia due to
lymphoma or granulomatous diseases. Dialysis is generally reserved for those with severe
hypercalcemia complicated with
kidney failure.