Hypercalcemia of malignancy is due to increased production of parathyroid hormone-related peptide from various tumor cells that initiate bone resorption and increased renal Ca2+ absorption. It can also be due to osteolysis from bone metastasis.7 It is generally severe and is a common cause of hypercalcemia in the inpatient setting.
Meticulous evaluation is vital to diagnose PHPT. Measurement of serum ionized Ca2+ reflects the biologically active Ca2+. Studies by Ong and colleagues suggest that about 24% of patients with the histologically proven parathyroid disease had isolated ionized hypercalcemia.8 It is also an important adjunct to diagnose the presumed normocalcemic PHPT in which both the ionized Ca2+ levels and serum total Ca2+ levels should be normal.9
In patients with hypoalbuminemia, a corrected serum Ca2+ is calculated using the equation: corrected Ca2+ = [0.8 × (normal albumin-patient’s albumin)] + serum Ca2+ level.
Serum PTH
Second-generation PTH assays (intact PTH) and third-generation PTH assays (bioactive PTH) are equally reliable in diagnosing PHPT.10 The results obtained with intact and bioactive PTH assays are highly correlated. Several studies have found no improvement in diagnostic accuracy when using the bioactive PTH assay.11,12
Serum PTH can be low, normal, or elevated in hypercalcemia. Hypercalcemia with a high PTH level is parathyroid-dependent hypercalcemia, whereas hypercalcemia with a suppressed PTH level is considered parathyroid-independent.
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