A complete history and physical examination and a review of the medical records are the most important elements in the emergency diagnosis of hypercalcemic crisis.9 Patients with PHPT rarely experience hypercalcemic crisis, and those who do usually have a long-standing history of progressive symptoms of hypercalcemia. Most patients presenting with hypercalcemia secondary to malignancy have an antecedent diagnosis of malignancy, and many are already hospitalized when severe hypercalcemia develops.

A serum calcium assay should be performed in all patients who present with psychological disturbances, renal insufficiency, cardiac dysrhythmias, and neurologic abnormalities.9

The most accurate and useful laboratory test for ruling out hypercalcemia is the ionized calcium assay,9 but most hospitals measure total serum calcium (ionized plus protein-bound calcium) unless the ionized calcium level is requested. If an ionized calcium assay is not available, total serum calcium may be measured and the value corrected for the measured albumin level.

The most specific laboratory test in the differential diagnosis of hypercalcemia is the serum intact PTH assay.27 An increased intact PTH level and calcium level are almost pathognomonic of HPT. Before the radioimmunoassay for intact PTH became available, the PTH assays in common use measured the PTH C-terminal or midregional fragment.9 Although detection of an elevated intact PTH level is a useful means of diagnosing PHT, the test usually takes a few days to complete and is of no immediate use in the management of hypercalcemic crisis. The quick intact PTH assay developed by Irvin and colleagues,28 however, has allowed rapid differential diagnosis of hypercalcemic crisis. It is an immunochemiluminometric assay and has a turnaround time of only 10 minutes.29 Conditions besides PHPT in which the intact PTH level is increased include hypocalcemia, secondary HPT (with low to low-normal serum calcium), and tertiary HPT (with normal to increased serum calcium) after a history of long-standing renal insufficiency.9 The intact PTH levels in patients with secondary HPT are characteristic of the patient-to-patient variability of the half-life of intact PTH and its molecular heterogeneity and biphasic metabolism.3031

Hypercalcemia secondary to malignancy occurs in patients whose diagnosis of malignancy is already established.3 Most patients who present with nonparathyroid hypercalcemia have malignant disease. It is important to establish whether the patient has HHM or skeletal metastases. Hypercalcemia develops before death from the malignancy in 30% of patients with carcinoma of the breast, 10% of patients with squamous cell carcinoma of the lung, and smaller percentages of patients with carcinoma of the esophagus, skin, kidney, pancreas, liver, colon, and ovary.9,10 Reliable assays for PTHrP are now available, but it takes several days to obtain the results, and they cannot be relied on as an adjunct to the emergency management of hypercalcemia.9 If the PTHrP levels are low, other osteolytic factors may be produced by the tumor, and other cases are associated with the production of interleukin-1, -6, or -11; transforming growth factor a or (3; interferon; or granulocyte-macrophage colony-stimulating factor.10

Paraneoplastic production of ectopic PTH is extremely rare.32 If familial hypocalciuric hypercalcemia (FHH) is suspected, an above-normal 24-hour urine calcium or a calcium clearance-to-creatinine ratio greater than 0.01 in patients who have never been documented to be normocalcemic rules out FHH.1 The serum 25-OH vitamin D level may be checked if excessive vitamin D intake is suspected. The serum l,25(OH)2 vitamin D level is high normal or mildly elevated in patients with PHPT. A cost-effective and accurate diagnosis of HPT can be made by documenting increased calcium and intact PTH levels in patients who are not hypocalciuric.

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