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Parathyroid hormone (PTH) interpretation of PTH results

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

Parathyroid hormone (PTH)

  • produced and secreted by the parathyroid glands
    • located along the posterior aspect of the thyroid gland
  • PTH is synthesized as a 115-amino acid precursor (pre-pro-PTH)
    • pre-pro-PTH is cleaved to pro-PTH and then to the 84-amino acid molecule, PTH (numbering starts at the amino-terminus)
    • precursor forms usually remain within the parathyroid cells
  • secreted PTH undergoes cleavage and metabolism to form:
    • carboxyl-terminal fragments (PTH-C)
      • 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
    • amino-terminal fragments (PTH-N)
      • only those portions of the molecule that carry the amino terminus (ie, the whole molecule and PTH-N) are biologically active
        • active forms have half-lives of approximately 5 minutes
    • mid-molecule fragments (PTH-M)

Calcium and PTH secretion

  • serum calcium level regulates PTH secretion via negative feedback through the parathyroid calcium sensing receptor (CASR)
    • reduced 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
        • enhances mobilization of calcium from bone and increasing renal synthesis of 1,25-dihydroxy vitamin D (this then increases intestinal calcium absorption)

Interpretation of PTH results

Parathyroid hormone (PTH) values should be interpreted in conjunction with serum calcium, magnesium, phosphate levels and creatinine levels, and the overall clinical presentation and history of the patient

  • raised PTH and raised calcium
    • about 90% of the patients with primary hyperparathyroidism have elevated parathyroid hormone (PTH) levels
      • remaining patients have normal (inappropriate for the elevated calcium level) PTH levels
      • the majority of patients will also have a reduced phosphate
    • 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 parathyroid calcium sensing receptor (CASR) mutations

  • low PTH, raised phosphate, raised calcium
    • if there is an (appropriately) low PTH level and high phosphate level in a hypercalcaemic patient
      • this is suggestive that the hypercalcaemia is not caused by PTH or PTH-like substances

  • low PTH, low phosphate, raised calcium
    • an (appropriately) low PTH level, low phosphate, raised calcium
      • suggestive of diagnosis of paraneoplastic hypercalcemia caused by parathyroid related peptide (PTHRP)
        • can transactivate the PTH receptor
        • can be produced by many different tumour types

  • low or normal PTH, low calcium
    • suggestive of hypoparathyroidism, provided the serum magnesium level is normal
    • low magnesium levels inhibit the release and action of PTH
      • therefore can mimic hypoparathyroidism

  • high PTH and low calcium
    • secondary hyperparathyroidism may occur in response to hypocalcemia or hyperphosphatemia
      • most commonly observed in renal failure
      • secondary hyperparathyroidism can also be caused by malabsorption of calcium due to intestinal disease and vitamin D deficiency
      • chronic secondary hyperparathyroidism develop high serum calcium and still have high PTH; this is tertiary hyperparathyroidism
    • if normal renal function then biochemical profile may be also due to resistance to PTH action (pseudohypoparathyroidism) or, very rarely, bio-ineffective PTH

  • high calcium, high PTH in advanced renal failure - this is tertiary hyperparathyroidism

Notes about interpretation of PTH levels:

  • if there is an elevated PTH value with a normal serum calcium
    • this is not necessarily due to primary hyperparathyroidism
    • the elevation in PTH may be due to secondary causes, the most likely being vitamin D deficiency
  • PTH levels vary during the day
    • the peak in PTH levels is about 2 a.m
    • PTH is usually measured at about 8 a.m
  • drugs that may increase PTH levels include phosphates, anticonvulsants, steroids, isoniazid, lithium, and rifampin
  • patients with high normal serum calcium (top end reference range) with raised PTH
    • may have primary hyperparathyroidism masked by vitamin D deficiency so must check always or early primary hyperparathyroidism/phenomenon called 'normocalcaemic hyperparathyroidism'. Natural history not well characterised
  • measurement of PTH
    • there are many fragments of PTH and tests for PTH may measure one or more of the fragments
      • none of the assays for intact PTH measure PTH (35-84), which is actually the fragment of PTH present in highest amounts in blood
        • many intact PTH assays measure PTH (7-84) as well
          • in the majority of people, this fragment is present in much lower amounts than PTH (1-84), so this is not a concern
            • however in renal failure, a common setting for measuring PTH levels, PTH (7-84) levels increase compared to PTH (1-84), and sometimes over half of what is measured as PTH represents this N-terminal truncated fragment. Some intact PTH assays do not measure this fragment and will give lower PTH results when increased PTH (7-84) is present
    • there are method related differences in PTH assays used across the UK. Therefore PTH results from different labs may not be comparable
    • PTH is a relatively unstable hormone which breaks down in blood after venepuncture but is stable for 48 hours in EDTA


  1. Fraser WD. Hyperparathyroidism. Lancet 2009; 374:145-58.
  2. Khan AA, Bilezikian JP, Potts JT Jr The diagnosis and management of asymptomatic primary hyperparathyroidism revisited. J Clin Endocrinol Metab 2009; 94:333-4

Additional Contributions from:

  • Dr Berenice Lopez, Consultant Chemical Pathologist, Harrogate and District NHS Foundation Trust (July 2012)

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