Interpretation

Approximately 90% of the patients with primary hyperparathyroidism have elevated parathyroid hormone (PTH) levels. The remaining patients have normal (inappropriate for the elevated calcium level) PTH levels. Approximately 40% of the patients with primary hyperparathyroidism have serum phosphorus levels below 2.5 mg/dL, and about 80% have serum phosphorus levels below 3.0 mg/dL.

A (appropriately) low PTH level and high phosphorus level in a patient with hypercalcemic suggests that the hypercalcemia is not caused by PTH or PTH-like substances.

A (appropriately) low PTH level with a low phosphorus level in a patient with hypercalcemia suggests the diagnosis of paraneoplastic hypercalcemia caused by parathyroid-related peptide (PTHRP). PTHRP shares N-terminal homology with PTH and can transactivate the PTH receptor. It can be produced by many different tumor types.

A low or normal PTH in a patient with hypocalcemia suggests hypoparathyroidism, provided the serum magnesium level is normal. Low magnesium levels inhibit PTH release and action and can mimic hypoparathyroidism.

Low serum calcium and high PTH levels in a patient with normal kidney function suggest resistance to PTH action (pseudohypoparathyroidism type 1a, 1b, 1c, or 2) or, very rarely, bio-ineffective PTH.

A limited number of the PTH-C fragments, which accumulate in kidney failure, chiefly PTH 7-84, cross-react in this and other intact PTH assays. PTH 1-84 is also elevated in kidney failure, with mild elevations being considered beneficial. Consequently, when measured with an intact PTH assay, concentrations of 1.5 to 3 times the upper limit of the healthy reference range appear to represent the optimal range for patients with kidney failure. Lower concentrations may be associated with adynamic renal bone disease, while higher levels suggest possible secondary or tertiary hyperparathyroidism, which can result in high-turnover renal osteodystrophy.

Some patients with moderate hypercalcemia and equivocal phosphate levels, who have either mild elevations in PTH or (inappropriately) normal PTH levels, may be suffering from familial hypocalciuric hypercalcemia, which is due to inactivating CASR genetic variants. The molar renal calcium to creatinine clearance is typically less than 0.01 in these individuals. The condition can be confirmed by CASR gene sequencing; see CASRG / CASR Full Gene Sequencing with Deletion/Duplication, Varies.