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Test Code PTH2P Parathyroid Hormone (PTH), with Minerals, Serum

Reporting Name

PTH with Minerals, S

Useful For

Diagnosis and differential diagnosis of hypercalcemia

 

Diagnosis of primary, secondary, and tertiary hyperparathyroidism

 

Diagnosis of hypoparathyroidism

 

Monitoring endstage renal failure patients for possible renal osteodystrophy

Profile Information

Test ID Reporting Name Available Separately Always Performed
PTH2 Parathyroid Hormone (PTH), S Yes Yes
CALS Calcium, Total, S No Yes
PHOI2 Phosphorus (Inorganic), S No Yes
CRET2 Creatinine, S No Yes

Performing Laboratory

Mayo Medical Laboratories in Rochester

Specimen Type

Serum


Specimen Required


Collection Container/Tube: 

Preferred: Serum gel

Acceptable: Red top

Submission Container/Tube: Plastic vial

Specimen Volume: 1 mL

Collection Instructions: Fasting (12 hours)

Additional Information: 12 hours before this blood test do not take multivitamins or dietary supplements containing biotin or vitamin B7, which are commonly found in hair, skin, and nail supplements and multivitamins.


Specimen Minimum Volume

0.5 mL

Specimen Stability Information

Specimen Type Temperature Time
Serum Frozen (preferred) 90 days
  Refrigerated  24 hours

Reference Values

PARATHYROID HORMONE

15-65 pg/mL

Reference values apply to all ages.

 

CALCIUM

Males

0-11 months: not established*

1-14 years: 9.6-10.6 mg/dL

15-16 years: 9.5-10.5 mg/dL

17-18 years: 9.5-10.4 mg/dL

19-21 years: 9.3-10.3 mg/dL

≥22 years: 8.9-10.1 mg/dL

Females

0-11 months: not established*

1-11 years: 9.6-10.6 mg/dL

12-14 years: 9.5-10.4 mg/dL

15-18 years: 9.1-10.3 mg/dL

≥19 years: 8.9-10.1 mg/dL

 

PHOSPHORUS

Males

0-11 months: not established**

1-4 years: 4.3-5.4 mg/dL

5-13 years: 3.7-5.4 mg/dL

14-15 years: 3.5-5.3 mg/dL

16-17 years: 3.1-4.7 mg/dL

≥18 years: 2.5-4.5 mg/dL

Females

0-11 months: not established**

1-7 years: 4.3-5.4 mg/dL

8-13 years: 4.0-5.2 mg/dL

14-15 years: 3.5-4.9 mg/dL

16-17 years: 3.1-4.7 mg/dL

≥18 years: 2.5-4.5 mg/dL

 

CREATININE

Males

0-11 months: not established

1-2 years: 0.1-0.4 mg/dL

3-4 years: 0.1-0.5 mg/dL

5-9 years: 0.2-0.6 mg/dL

10-11 years: 0.3-0.7 mg/dL

12-13 years: 0.4-0.8 mg/dL

14-15 years: 0.5-0.9 mg/dL

≥16 years: 0.8-1.3 mg/dL

Females

0-11 months: not established

1-3 years: 0.1-0.4 mg/dL

4-5 years: 0.2-0.5 mg/dL

6-8 years: 0.3-0.6 mg/dL

9-15 years: 0.4-0.7 mg/dL

≥16 years: 0.6-1.1 mg/dL

 

*The serum concentration of calcium varies significantly during the immediate neonatal period. In general, the serum calcium concentration decreases over the first days of life, followed by a gradual increase to adult concentrations by the second or third week of life.

**The plasma concentrations of inorganic phosphate in the neonatal period can be greater than those of the adult.

Day(s) and Time(s) Performed

Monday through Friday; 5 a.m.-12 a.m., Saturday; 6 a.m.-6 p.m.

Test Classification

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

82310-Calcium

82565-Creatinine

83970-PTH

84100-Phosphorus

LOINC Code Information

Test ID Test Order Name Order LOINC Value
PTH2P PTH with Minerals, S In Process

 

Result ID Test Result Name Result LOINC Value
CALS Calcium, Total, S 17861-6
CRET2 Creatinine, S 2160-0
PHOI2 Phosphorus (Inorganic), S 2777-1
PTH2 Parathyroid Hormone (PTH), S 2731-8

Clinical Information

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.

Interpretation

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, bioineffective 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 (CSRSP / Calcium Sensing Receptor [CASR] Gene, Full Gene Analysis).

Clinical Reference

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

Analytic Time

Same day/1 day

Reject Due To

Hemolysis

Mild reject; Gross reject

Lipemia

Mild OK; Gross OK

Icterus

NA

Other

NA

Method Name

PTH2: Electrochemiluminescence

CALS: Photometric, O-Cresolphthalein

PHOI2: Photometric, Ammonium Molybdate

CRET2: Enzymatic Colorimetric Assay