Parathyroid hormone (PTH)
Sample
- The serum of the patient is required.
- A fasting sample is preferred.
- Place on ice.
- The serum should be separated immediately because the PTH is unstable at room temperature and even on refrigeration.
- Refrigerate during centrifugation.
- Immediately freeze the sample.
- Can store at -20 °C to -70 ° C.
- A lower level has seen if the sample left at room temperature even for 4 hours.
- Also, a lower level has seen if the sample is kept at 4 °C for one day.
- If the chemical method allows then the EDTA plasma is the best choice.
- Simultaneous estimation of total calcium, ionized calcium, and phosphorus is recommended
Purpose of the test (Indications)
- This is done to evaluate hypercalcemia or hypocalcemia.
- This is also done to establish the diagnosis of hyperparathyroidism.
- PTH differentiates hyperparathyroidism from Nonparathyroid causes leading to hypercalcemia.
Precaution
- lipemic serum and hemolysis interfere with the method.
- Some drugs may affect the result and increase PTH value like:
- Anticonvulsants.
- Isoniazid.
- Lithium.
- Rifampicin.
- Steroids.
- Drugs which decrease PTH are:
- Cimetidine.
- Propranolol.
Pathophysiology
- This is a polypeptide hormone produced in the parathyroid gland.
- These 4 in number and present close to or on the posterior surface of the thyroid gland.
- Additional parathyroid glands may be found in the mediastinum (in thymus gland) or neck.
- Formation of PTH:
- Preparathyroid (115 AA) is synthesized in the ribosomes of Cheif cells.
- By proteolysis converted into Pro-PTH (90 AA).
- By the second proteolysis converted into Intact-PTH (1- 84 AA).
- PTH-1-84 is metabolized in the peripheral tissue mainly the liver and kidney.
- This is stored in the gland and some of it goes into blood circulation.
- The biological activity of the PTH resides in the first 30 AA of the N-terminal.
- The concentration of the biologically active form of PTH is very low in the blood circulation (10 pmol/L or 0.1 ng/mL).
- PTH secretion is directly controlled by plasma calcium.
- This is the main hormone to regulate the concentration of Calcium in the extracellular fluid.
- A decrease in the ionized calcium is the stimulus for the PTH secretion.
- PTH + 1,25- hydroxy D3 rais the calcium level by the following mechanisms:
- It promotes dissolving of the bone.
- Increases renal tubular reabsorption of calcium in the kidney.
- Increase intestinal absorption of the calcium.
- A rise in Calcium inhibits PTH secretion.
- Magnesium also influences the PTH level.
- Hypermagnesemia suppresses the PTH secretion, although not like Calcium.
Clinical condition | PTH | PTH |
Ionized hypocalcemia | Stimulate | |
Ionized hypercalcemia | Suppress | |
Hyperphosphatemia | stimulate | |
Hypermagnesemia | Suppress |
- Primary hyperparathyroidism is caused by parathyroid adenoma or rarely by cancer.
- The patient will have high PTH.
- and high Calcium level.
- Secondary hyperparathyroidism is due to chronic renal failure where the patient has low calcium and high phosphate.
- Now parathyroid glands persistently produce PTH to maintain Calcium level.
- These patients have high PTH and low calcium.
- Tertiary hyperparathyroidism In this case patients bypasses the compensatory mechanism.
- Develops a high PTH level.
- This PTH leads to hypercalcemia.
- These patients have high PTH and High calcium levels.
- Intact PTH molecule metabolized to three different molecules:
- N-terminal.
- Mid-Region.
- C- terminal.
- PTH level has diurnal variation. it is the highest at around 2 AM and lowest at around 2 PM.
Normal
Source 1
C- terminal and midmolecule
- Serm (by RIA)
- 1 to 16 years = 51 to 217 pg/mL
- Adult = 50 to 300 pg/mL
N- Terminal
- Serum (by RIA)
- 2 to 13 year = 14 to 21 pg/mL
- Adult = 8 to 24 pg/mL
Intact molecule
- Serum (by ICMA))
- Cord blood = ≤ 3 pg/mL
- 2 to 20 year = 9 to 52 pg/mL
- Adult = 10 to 65 pg/mL
Source 2
- Intact PTH molecule = 10 to 65 pg/mL (10 to 65 ng/mL)
- N-terminal intact PTH = 8 to 24 pg/L (8 to 24 ng/L)
- C-terminal intact PTH = 50 to 330 pg/L (50 to 330 ng/L)
- Mostly the intact PTH molecule is recommended.
Increased PTH level is seen in:
- Primary hyperparathyroidism.
- Pseudohypoparathyroidism ( Secondary hyperparathyroidism ).
- Vit. D deficiency ( hereditary ) and rickets.
- Zollinger Ellison syndrome.
- Non-PTH producing tumors give rise to the paraneoplastic syndrome, They produce PTH like protein which acts like PTH.
- Chronic renal failure.
- Hypocalcemia.
- Malabsorption.
Decreased PTH level is seen in:
- Grave’s disease ( Hypoparathyroidism ).
- Non-Parathyroid hypercalcemia.
- Surgical, secondary hypoparathyroidism.
- Sarcoidosis.
- Metastatic bone tumors.
- Vit.D intoxication.
- Milk-alkali syndrome.
- DiGeorge syndrome.
good informations
Thanks for the encouraging remarks