Parathyroid Hormone (PTH), Serum
NY State Approved Indicates the status of NY State approval and if the test is orderable for NY State clients.
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
Reporting Name A shorter/abbreviated version of the Published Name for a test; an abbreviated test name
Parathyroid Hormone (PTH), S
Intact PTH (Parathyroid Hormone)
PTH (Parathyroid Hormone)
PTH (Parathyroid Hormone)
Specimen Type Describes the specimen type needed for testing
Specimen Required Defines the optimal specimen. This field describes the type of specimen required to perform the test and the preferred volume to complete testing. The volume allows automated processing, fastest throughput and, when indicated, repeat or reflex testing.
Preferred: Red top
Acceptable: Serum gel
Submission Container/Tube: Plastic vial
Specimen Volume: 1 mL
Collection Instructions: Fasting (12 hours)
Specimen Minimum Volume Defines the amount of specimen required to perform an assay once, including instrument and container dead space. Submitting the minimum specimen volume makes it impossible to repeat the test or perform confirmatory or perform reflex testing. In some situations, a minimum specimen volume may result in a QNS (quantity not sufficient) result, requiring a second specimen to be collected.
Mild reject; Gross reject
Mild OK; Gross OK
Specimen Stability Information Provides a description of the temperatures required to transport a specimen to the laboratory. Alternate acceptable temperature(s) are also included.
|Serum||Frozen (preferred)||90 days|
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 >90% of the total circulating PTH and are primarily cleared by the kidneys. In patients with renal failure, PTH-C fragments can accumulate to 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 mutations.
Hypoparathyroidism is most commonly secondary to thyroid surgery, but can also occur on an autoimmune basis, or due to activating CASR mutations. 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.
Reference values apply to all ages.
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 <2.5 mg/dL and about 80% have serum phosphorus <3.0 mg/dL.
An (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.
An (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 mutations. The molar renal calcium to creatinine clearance is typically <0.01 in these individuals. The condition can be confirmed by CASR gene mutation screening (CSRMS/83703 Calcium Sensing Receptor [CASR] Gene, Mutation Screen).
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 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 who have been 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.
In patients receiving high dose (>5 mg/day) biotin therapy, the specimen should be collected at least 8 hours after the last biotin administration.
Clinical Reference Provides recommendations for further in-depth reading of a clinical nature
1. Boudou P, Ibrahim F, Cormier C, et al: 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, et al: 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 hypoparathyroidism. 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
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(a) 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: Roche PTH reagent, Roche Diagnostics Corp, Indianapolis, IN November 2006)
Day(s) and Time(s) Test Performed Outlines the days and times the test is performed. This field reflects the day and time the sample must be in the testing laboratory to begin the testing process and includes any specimen preparation and processing time required before the test is performed. Some tests are listed as continuously performed, which means assays are performed several times during the day.
Monday through Friday; 5 a.m.-12 a.m., Saturday; 6 a.m.-6 p.m.
Analytic Time Defines the amount of time it takes the laboratory to setup and perform the test. This is defined in number of days. The shortest interval of time expressed is "same day/1 day," which means the results may be available the same day that the sample is received in the testing laboratory. One day means results are available 1 day after the sample is received in the laboratory.
Same day/1 day
Maximum Laboratory Time Defines the maximum time from specimen receipt at Mayo Medical Laboratories until the release of the test result
Specimen Retention Time Outlines the length of time after testing that a specimen is kept in the laboratory before it is discarded
Performing Laboratory Location The location of the laboratory that performs the test
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's instructions, or as products that do not undergo full FDA review and approval, and are then labeled as an Analyte Specific Reagent (ASR), Investigation Use Only (IUO) product, or a Research Use Only (RUO) product.
This test has been cleared or approved by the U.S. 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 Medical Laboratories interpretation of CPT coding requirements. It is the responsibility of each laboratory to determine correct CPT codes to use for billing.
LOINC® Code Information Provides guidance in determining the Logical Observation Identifiers Names and Codes (LOINC) values for the result codes returned for this test or profile.
|Result ID||Reporting Name||LOINC Code|
|PTH2||Parathyroid Hormone (PTH), S||In Process|