Test Catalog

Test ID: PTH2    
Parathyroid Hormone, Serum

Useful For Suggests clinical disorders or settings where the test may be helpful

Diagnosis and differential diagnosis of hypercalcemia


Diagnosis of primary, secondary, and tertiary hyperparathyroidism


Diagnosis of hypoparathyroidism


Monitoring end-stage renal failure patients for possible renal osteodystrophy

Clinical Information Discusses physiology, pathophysiology, and general clinical aspects, as they relate to a laboratory test

Parathyroid hormone (PTH) is produced and secreted by the parathyroid glands, which are located along the posterior aspect of the thyroid gland. The hormone is synthesized as a 115-amino acid precursor (pre-pro-PTH), cleaved to pro-PTH, and then to the 84-amino acid molecule, PTH (numbering, by universal convention, starting at the amino terminus). The precursor forms generally remain within the parathyroid cells.


Secreted PTH undergoes cleavage and metabolism to form carboxyl-terminal fragments (PTH-C), amino-terminal fragments (PTH-N), and mid-molecule fragments (PTH-M). Only those portions of the molecule that carry the amino-terminus (ie, the whole molecule and PTH-N) are biologically active. The active forms have half-lives of approximately 5 minutes. The inactive PTH-C fragments, with half-lives of 24 to 36 hours, make up more than 90% of the total circulating PTH and are primarily cleared by the kidneys. In patients with renal failure, PTH-C fragments can accumulate to very high levels. PTH 1-84 is also elevated in these patients, with mild elevations being considered a beneficial compensatory response to end organ PTH resistance, which is observed in renal failure.


The serum calcium level regulates PTH secretion via negative feedback through the parathyroid calcium sensing receptor (CASR). Decreased calcium levels stimulate PTH release. Secreted PTH interacts with its specific type II G-protein receptor, causing rapid increases in renal tubular reabsorption of calcium and decreased phosphorus reabsorption. It also participates in long-term calciostatic functions by enhancing mobilization of calcium from bone and increasing renal synthesis of 1,25-dihydroxy vitamin D, which, in turn, increases intestinal calcium absorption. In rare inherited syndromes of parathyroid hormone resistance or unresponsiveness, and in renal failure, PTH release may not increase serum calcium levels.


Hyperparathyroidism causes hypercalcemia, hypophosphatemia, hypercalcuria, and hyperphosphaturia. Long-term consequences are dehydration, renal stones, hypertension, gastrointestinal disturbances, osteoporosis, and sometimes neuropsychiatric and neuromuscular problems. Hyperparathyroidism is most commonly primary and caused by parathyroid adenomas. It can also be secondary in response to hypocalcemia or hyperphosphatemia. This is most commonly observed in renal failure. Long-standing secondary hyperparathyroidism can result in tertiary hyperparathyroidism, which represents the secondary development of autonomous parathyroid hypersecretion. Rare cases of mild, benign hyperparathyroidism can be caused by inactivating CASR genetic variants.


Hypoparathyroidism is most commonly secondary to thyroid surgery, but can also occur on an autoimmune basis, or due to activating CASR genetic variants. The symptoms of hypoparathyroidism are primarily those of hypocalcemia, with weakness, tetany, and possible optic nerve atrophy.

Reference Values Describes reference intervals and additional information for interpretation of test results. May include intervals based on age and sex when appropriate. Intervals are Mayo-derived, unless otherwise designated. If an interpretive report is provided, the reference value field will state this.

<1 month: 7.0-59 pg/mL

4 weeks-11 months: 8.0-61 pg/mL

12 months-10 years: 11-59 pg/mL

11 years-17 years: 15-68 pg/mL

18 years and older: 15-65 pg/mL

Interpretation Provides information to assist in interpretation of the test results

About 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. About 40% of the patients with primary hyperparathyroidism have serum phosphorus levels below 2.5 mg/dL, and about 80% have serum phosphorus below 3.0 mg/dL.


A (appropriately) low PTH level and high phosphorus level in a hypercalcemic patient 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 hypercalcemic patient 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 renal 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 renal failure, chiefly PTH 7-84, cross-react in this and other intact PTH assays. PTH 1-84 is also elevated in renal 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 end-stage renal failure patients. 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 CASRZ / CASR Gene, Full Gene Analysis, Varies.

Cautions Discusses conditions that may cause diagnostic confusion, including improper specimen collection and handling, inappropriate test selection, and interfering substances

Parathyroid hormone (PTH) values should be interpreted in conjunction with serum calcium and phosphorus levels, and the overall clinical presentation and history of the patient.


Do not interpret an elevated PTH value with a normal serum calcium result as necessarily indicative of primary hyperparathyroidism. It is possible that the elevation in PTH is due to secondary causes, the most likely being vitamin D deficiency.


Normal reference ranges may vary based on geographical locations of the populations studied.


The carboxyl-terminal fragments (PTH-C) fragment 7-84, which accumulates in renal failure, shows substantial cross-reactivity in this assay. Healthy population reference ranges, therefore, do not apply in renal failure.


As with all tests containing monoclonal mouse antibodies, erroneous findings may be obtained from specimens taken from patients previously treated with monoclonal mouse antibodies or have received them for diagnostic purposes.


In rare cases, interference due to extremely high titers of antibodies to ruthenium or streptavidin can occur.

Clinical Reference Recommendations for in-depth reading of a clinical nature

1. Boudou P, Ibrahim F, Cormier C, Chabas A, Sarfati E, Souberbielle JC: Third- or second-generation parathyroid hormone assays: a remaining debate in the diagnosis of primary hyperparathyroidism. J Clin Endocrinol Metab. 2005;90(12):6370-6372

2. Silverberg SJ, Bilezikian JP: The diagnosis and management of asymptomatic primary hyperparathyroidism. Nat Clin Pract Endocrinol Metab. 2006;2(9):494-503

3. Brossard JH, Cloutier M, Roy L, Lepage R, Gascon-Barre M, D'Amour P: Accumulation of a non-(1-84) molecular form of parathyroid hormone (PTH) detected by intact PTH assay in renal failure: importance in the interpretation of PTH values. J Clin Endocrinol Metab. 1996;81:3923-3929

4. Garfield N, Karaplis AC: Genetics and animal models of hypo-parathyroidism. Trends Endocrinol Metab. 2001;12:288-294

5. Sakhaee K: Is there an optimal parathyroid hormone level in end-stage renal failure: the lower the better? Curr Opin Nephrol Hypertens. 2001;10:421-427

6. Vetter T, Lohse MJ: Magnesium and the parathyroid. Curr Opin Nephrol Hypertens. 2002;11:403-410

7. Bilezikian JP, Potts JT Jr, Fuleihan Gel-H, et al: Summary statement from a workshop on asymptomatic primary hyperparathyroidism: a perspective for the 21st century. J Clin Endocrinol Metab. 2002;87:5353-5361

8. Minisola S, Pepe J, Piemonte S, Cipriani C: The diagnosis and management of hypercalcaemia. BMJ. 2015 Jun;350:h2723

9. Cooper MS: Disorders of calcium metabolism and parathyroid disease. Best Pract Res Clin Endocrinol Metab. 2011 Dec;25(6):975-983. doi: 10.1016/j.beem.2011.07.001

10. De Sanctis V, Soliman A, Fiscina B: Hypoparathyroidism: from diagnosis to treatment. Curr Opin Endocrinol Diabetes Obes. 2012 Dec;19(6):435-442. doi: 10.1097/MED.0b013e3283591502