Updated: Aug 21, 2025
The reference ranges for parathyroid hormone (PTH) are as follows:
PTH levels in the blood may be analyzed to determine the presence of Hyperparathyroidism (primary, secondary, or tertiary), pseuodohypoparathyroidism, or hypoparathyroidism and its possible role in abnormal calcium levels.
PTH is not typically a part of a panel and should be ordered specifically.
PTH is produced by the four parathyroid glands, which reside behind the thyroid gland in the anterior neck. A portion of PTH is split into three fragments in the parathyroid gland before systemic release. The three fragments are an amino or N-terminal fragment, a mid-region fragment, and a carboxy or C-terminal fragment. The active intact PTH and the amino terminal fragment are physiologically active in the body. In some centers, assays are available to detect both active elements. PTH influences the levels of both calcium and phosphorus in the body. The release of PTH is normally stimulated by low calcium levels in the body. PTH release results in a signal to the bones to release calcium into the bloodstream and also to the kidneys to resorb calcium in the collecting system and excrete phosphorus.
In addition, PTH plays an indirect role in the intestines, by stimulating the conversion of vitamin D into its active form (25-hydroxy vitamin D to 1,25-dihydroxy vitamin D in the proximal renal tubules), which then stimulates the intestines to absorb both calcium and phosphorus.
Conversely, elevated levels of serum ionized calcium serve as a negative-feedback loop for PTH secretion by triggering the calcium sensing receptor on the surface of the parathyroid cells, suppressing PTH gene expression and proliferation of parathyroid cells, eventually inhibiting PTH secretion. This allows for excretion of excess calcium from the body. In the instance of renal disease or parathyroid disease, this normal mechanism runs awry, and the result can be injurious to multiple body systems, including the bones, muscles, kidneys, and brain function.
PTH levels are helpful in identifying the underlying cause of calcium aberrations. This may delineate hyperparathyroidism, parathyroid tumors, vitamin D deficiency, renal disease, and some tumors that produce the hormone. Intraoperative PTH assays may be performed during parathyroid tumor surgery to help determine if the PTH-producing adenoma was correctly removed.
A drop of more than 50% in the preoperative level 10 min after gland removal can be confirmation that the correct gland with the PTH-producing adenoma was removed. If the level does not drop by 50% and ends up in the normal range, another source should be sought. Some authors suggest waiting for 20 min to avoid unnecessary bilateral neck exploration and the associated risk for complications with only a slight increase in the duration of surgery and costs due to variations in individual PTH half-life and alterations in the patient's physiological state during surgery.
Often, in conditions in which abnormal calcium levels are detected, PTH may be drawn and interpreted along with Serum Calcium, phosphorus, magnesium, vitamin D, and Urine Calcium levels. In cases of suspected hypercalcemia due to malignancy, serum levels of parathyroid hormone–related protein may be measured. The understanding of PTH in relation to the other listed labs may allow for an appropriate diagnosis of the underlying pathology.
Some authors recommend that samples for PTH measurement should be placed into tubes containing EDTA, at 10:00 AM and 4:00 PM, and plasma separated within 24 h of venipuncture. These recommendations are related to multiple differences noted in methods of collections: central venous PTH concentrations vs peripheral venous concentrations, storage collection temperature and time until analysis, and variations in levels related to a circadian rhythm (i.e., a nocturnal acrophase and midmorning nadir). Thus, for patients working in night shifts, it is advisable to consult with their health care provider/lab personnel prior to sample collection.
