Parathormone (PTH), a polypeptide hormone produced in the parathyroid gland, is one of the major factors in the regulation of calcium concentration in extracellular fluid. Three molecular forms of PTH exist: intact (also called native or glandular hormone), multiple N-terminal fragments, and C-terminal fragments. PTH follows a circadian rhythm pattern; highest values are between 2:00 and 4:00 p.m. (1400 and 1600 hours), and lowest values are at about 8:00 a.m. (0800 hours).
This test studies altered calcium metabolism, establishes a diagnosis of hyperparathyroidism, and distinguishes nonparathyroid from parathyroid causes of hypercalcemia. A decrease in the level of ionized calcium is the primary stimulus for PTH secretions, whereas a rise in calcium inhibits secretions. This normal relation is lost in hyperthyroidism, and PTH will be inappropriately high in relation to calcium. Acute changes in secretory activity are better reflected by the PTH and N-terminal assay. PTH and N-terminal levels are usually decreased when hypercalcemia is due to neoplastic secretions (prostaglandins). PTH and N-terminal levels may be a more reliable indication of secondary hyperparathyroidism in patients with renal failure. Creatinine level is determined concurrently with all PTH assays to determine kidney function and for meaningful interpretation of results.
N-terminal: 824 pg/mL or 824 ng/L
Intact molecule: 1065 pg/mL or 1065 ng/L
Calcium: 8.510.9 mg/dL (calcium must be tested to properly interpret results)
C-terminal (biomolecule): 50330 pg/mL or 50330 ng/L
Obtain a 10-mL venous blood sample (lavender-topped [EDTA] tube) from a patient who has fasted for 10 hours. Collect the sample in chilled vials and keep on ice. Observe standard precautions. Serum or EDTA is used.
Immediately take the specimen to the laboratory and centrifuge at 4 °C after blood has clotted.
Increased PTH values occur with:
Primary hyperparathyroidism
Pseudohyperparathyroidism when there is a primary defect in renal tubular responsiveness to PTH (secondary hyperparathyroidism)
Hereditary vitamin D deficiency
Zollinger-Ellison syndrome (increased production of gastrin as a result of a tumor in the pancreas)
CKD
Hypocalcemia
Spinal cord injury
Decreased PTH values occur in the following conditions:
Hypoparathyroidism (Graves disease)
Nonparathyroid hypercalcemia
Secondary hypoparathyroidism (surgical)
Magnesium deficiency
Sarcoidosis
Hyperthyroidism
DiGeorge syndrome (a disorder caused by a defect in chromosome 22 resulting in heart and immune system problems)
Increased PTHN-terminal values occur in the following conditions:
Primary hyperparathyroidism
Secondary hyperparathyroidism (more reliable than PTH and C-terminal)
Decreased PTHN-terminal values occur in the following conditions:
Hypoparathyroidism
Nonparathyroid hypercalcemia
Aluminum-associated osteomalacia
Severely impaired bone mineralization
Increased PTHC-terminal values occur in the following conditions:
Primary hyperparathyroidism (very specific for)
Some neoplasms with elevated calcium
Kidney failure (even if parathyroid disease is absent)
Decreased PTHC-terminal values occur in the following conditions:
Hypoparathyroidism
Nonparathyroid hypercalcemia
Pretest Patient Care
Explain test purpose and procedure.
Remind the patient that fasting for at least 10 hours is required. Draw blood by 8:00 a.m. (0800 hours) because of circadian rhythm changes. Concurrently, also draw blood for testing of calcium level.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal activities.
Review test results; report and record findings. Modify the nursing care plan as needed. Monitor appropriately for calcium imbalance and hypoparathyroidism or hyperparathyroidism.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
Elevated blood lipids and hemolysis interfere with test methods.
Milk-alkali syndrome (Burnett syndrome, hypercalcemia) may falsely lower PTH levels.
Recently administered radioisotopes (see Appendix E) will alter results.
Vitamin D deficiency will increase PTH levels.
Many drugs alter results; phosphates raise PTH levels up to 125%, and vitamin A and D overdoses decrease PTH levels (see Appendix E).
Lowering plasma calcium by 1.5 mg/dL or 0.38 nmol/L will result in a fourfold increase in PTH levels.