There are typically four parathyroid glands. As the name implies, they are located near the thyroid gland in the neck, although the number and particularly the location are quite variable. These pea-sized glands play a vital role in maintaining the body's calcium level. (See also Hypercalcemia and Hypocalcemia.)
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 within minutes of a fall in serum calcium concentration.
PTH increases serum calcium acutely 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
By this mechanism PTH causes plasma phosphate to fall as it raises calcium thus preventing precipitation of calcium phosphate in body tissues
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).
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 when advanced chronic kidney disease is present, second-generation assays that measure the intact PTH molecule are used. PTH increases urinary cyclic adenosine monophosphate (cAMP). Nephrogenous cAMP excretion is measured to diagnose pseudohypoparathyroidism.
