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 kidney failure patients for possible renal osteodystrophy

Method Name
A short description of the method used to perform the test


NY State Available
Indicates the status of NY State approval and if the test is orderable for NY State clients.


Reporting Name
Lists a shorter or abbreviated version of the Published Name for a test

Parathyroid Hormone (PTH), S

Lists additional common names for a test, as an aid in searching

Intact PTH (Parathyroid Hormone)

PTH (Parathyroid Hormone)

Specimen Type
Describes the specimen type validated for testing


Specimen Required
Defines the optimal specimen required to perform the test and the preferred volume to complete testing

Patient Preparation:

1. For 12 hours before specimen collection do not take multivitamins or dietary supplements containing biotin (vitamin B7), which is commonly found in hair, skin, and nail supplements and multivitamins.

2. Patient should be fasting for 12 hours

Collection Container/Tube:

Preferred: Serum gel

Acceptable: Red top

Submission Container/Tube: Plastic vial

Specimen Volume: 1 mL


If not ordering electronically, complete, print, and send a Renal Diagnostics Test Request (T830) with the specimen. 

Specimen Minimum Volume
Defines the amount of sample necessary to provide a clinically relevant result as determined by the Testing Laboratory

0.75 mL

Reject Due To
Identifies specimen types and conditions that may cause the specimen to be rejected

Gross hemolysis Reject
Gross lipemia OK

Specimen Stability Information
Provides a description of the temperatures required to transport a specimen to the performing laboratory, alternate acceptable temperatures are also included

Specimen Type Temperature Time Special Container
Serum Frozen (preferred) 180 days
Refrigerated 72 hours
Ambient 8 hours

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 kidney 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 kidney 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 kidney 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 kidney 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 kidney failure, PTH release may not increase serum calcium levels.


Hyperparathyroidism causes hypercalcemia, hypophosphatemia, hypercalcuria, and hyperphosphaturia. Long-term consequences are dehydration, kidney 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 kidney 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

Provides information to assist in interpretation of the test results

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 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 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 end-stage kidney 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 kidney 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.

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 (PTH-C) fragment 7-84, which accumulates in kidney failure, shows substantial cross-reactivity in this assay. Healthy population reference ranges, therefore, do not apply in kidney 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 Dec;90(12):6370-6372

2. Silverberg SJ, Bilezikian JP: The diagnosis and management of asymptomatic primary hyperparathyroidism. Nat Clin Pract Endocrinol Metab. 2006 Sep;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 Nov;81(11):3923-3929

4. Garfield N, Karaplis AC: Genetics and animal models of hypoparathyroidism. Trends Endocrinol Metab. 2001 Sep;12(7):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 May;10(3):421-427

6. Vetter T, Lohse MJ: Magnesium and the parathyroid. Curr Opin Nephrol Hypertens. 2002 Jul;11(4):403-410

7. Bilezikian JP, Potts JT Jr, Fuleihan GEH, et al: Summary statement from a workshop on asymptomatic primary hyperparathyroidism: a perspective for the 21st century. J Clin Endocrinol Metab. 2002 Dec;87(12):5353-5361

8. Minisola S, Pepe J, Piemonte S, Cipriani C: The diagnosis and management of hypercalcaemia. BMJ. 2015 Jun 2;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

Method Description
Describes how the test is performed and provides a method-specific reference

The Roche cobas assay for determining intact parathyroid hormone employs a sandwich test principle in which a biotinylated monoclonal antibody reacts with the N-terminal fragment (1-37) and a monoclonal antibody labeled with a ruthenium complex reacts with the C-terminal fragment (38-84). Application of a voltage to the electrode then induces chemiluminescent emission, which is measured by a photomultiplier. The antibodies used in this assay are reactive with epitopes in the amino acid regions 26-32 and 37-42.(Package insert: Elecsys PTH reagent. Roche Diagnostics; V 2.0 English, 02/2020)

PDF Report
Indicates whether the report includes an additional document with charts, images or other enriched information


Day(s) Performed
Outlines the days the test is performed. This field reflects the day that the sample must be in the testing laboratory to begin the testing process and includes any specimen preparation and processing time before the test is performed. Some tests are listed as continuously performed, which means that assays are performed multiple times during the day.

Monday through Saturday

Report Available
The interval of time (receipt of sample at Mayo Clinic Laboratories to results available) taking into account standard setup days and weekends. The first day is the time that it typically takes for a result to be available. The last day is the time it might take, accounting for any necessary repeated testing.

Same day/1 to 2 days

Specimen Retention Time
Outlines the length of time after testing that a specimen is kept in the laboratory before it is discarded

3 months

Performing Laboratory Location
Indicates the location of the laboratory that performs the test


Several factors determine the fee charged to perform a test. Contact your U.S. or International Regional Manager for information about establishing a fee schedule or to learn more about resources to optimize test selection.

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  • Prospective clients should contact their Regional Manager. For assistance, contact Customer Service.

Test Classification
Provides information regarding the medical device classification for laboratory test kits and reagents. Tests may be classified as cleared or approved by the US Food and Drug Administration (FDA) and used per manufacturer instructions, or as products that do not undergo full FDA review and approval, and are then labeled as an Analyte Specific Reagent (ASR) product.

This test has been cleared, approved, or is exempt by the US Food and Drug Administration and is used per manufacturer's instructions. Performance characteristics were verified by Mayo Clinic in a manner consistent with CLIA requirements.

CPT Code Information
Provides guidance in determining the appropriate Current Procedural Terminology (CPT) code(s) information for each test or profile. The listed CPT codes reflect Mayo Clinic Laboratories interpretation of CPT coding requirements. It is the responsibility of each laboratory to determine correct CPT codes to use for billing.

CPT codes are provided by the performing laboratory.


LOINC® Information
Provides guidance in determining the Logical Observation Identifiers Names and Codes (LOINC) values for the order and results codes of this test. LOINC values are provided by the performing laboratory.

Test Id Test Order Name Order LOINC Value
PTH2 Parathyroid Hormone (PTH), S 2731-8
Result Id Test Result Name Result LOINC Value
Applies only to results expressed in units of measure originally reported by the performing laboratory. These values do not apply to results that are converted to other units of measure.
PTH2 Parathyroid Hormone (PTH), S 2731-8

Test Setup Resources

Setup Files
Test setup information contains test file definition details to support order and result interfacing between Mayo Clinic Laboratories and your Laboratory Information System.

Excel | Pdf

Sample Reports
Normal and Abnormal sample reports are provided as references for report appearance.

Normal Reports | Abnormal Reports

SI Sample Reports
International System (SI) of Unit reports are provided for a limited number of tests. These reports are intended for international account use and are only available through MayoLINK accounts that have been defined to receive them.

SI Normal Reports | SI Abnormal Reports