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Overview of Parathyroid Function


James L. Lewis III

, MD, Brookwood Baptist Health and Saint Vincent’s Ascension Health, Birmingham

Last full review/revision Mar 2021| Content last modified Sep 2022
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Parathyroid cells manufacture, store, and secrete a polypeptide hormone called parathyroid hormone (PTH). PTH has several actions, but perhaps the most important is to

  • Increase serum calcium

Parathyroid cells sense decreases in serum calcium and, in response, release preformed PTH into the circulation.

PTH increases serum calcium within minutes by

  • Increasing renal and intestinal absorption of calcium

  • Rapidly mobilizing calcium and phosphate from bone by stimulating bone resorption

Renal calcium excretion generally parallels sodium excretion and is influenced by many of the same factors that govern sodium transport in the proximal tubule. However, PTH enhances distal tubular calcium reabsorption independently of sodium.

PTH also

  • Decreases renal phosphate reabsorption and thus increases renal phosphate losses

Renal phosphate loss prevents the solubility product of calcium and phosphate from being exceeded in plasma as calcium concentrations rise in response to PTH. PTH also increases serum calcium by stimulating conversion of vitamin D to its most active form, calcitriol (1,25-dihydroxycholecalciferol). This form of vitamin D increases the percentage of dietary calcium absorbed by the intestine. Despite increased calcium absorption, long-term increased secretion of PTH generally results in net bone resorption as osteoblastic function is inhibited and osteoclastic activity is promoted. PTH and vitamin D both function as important regulators of bone growth and bone remodeling (see also Vitamin D Deficiency and Dependency Vitamin D Deficiency and Dependency Inadequate exposure to sunlight predisposes to vitamin D deficiency. Deficiency impairs bone mineralization, causing rickets in children and osteomalacia in adults and possibly contributing... read more ).

PTH is rapidly cleared from the circulation by the liver, which cleaves the intact peptide into amino and carboxy terminal fragments. These fragments are then excreted by the kidneys. Radioimmunoassays for these fragments were the first tests available for diagnosing primary hyperparathyroidism and monitoring hyperparathyroidism secondary to renal disease, but because the PTH breakdown rate varies with calcium level and renal excretion can be decreased with advanced chronic kidney disease, second generation assays that measure the intact PTH molecule are now used. PTH increases urinary cyclic adenosine monophosphate (cAMP). Nephrogenous cAMP excretion is measured to diagnose pseudohypoparathyroidism.

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