What is "hyperparathyroidism"

n. (context medicine English) An abnormal increase in parathyroid gland activity

n. excessive secretion of parathyroid hormone resulting in abnormally high levels of calcium in the blood; can affect many systems of the body (especially causing bone resorption and osteoporosis) [ant: hypoparathyroidism]

Hyperparathyroidism is inappropriate overactivity of the parathyroid glands resulting in parathyroid hormone (PTH) levels in the blood above what a normally functioning plasma ionized calcium regulator (or homeostat, or negative feedback mechanism) would produce. Hyperparathyroidism can also result if the organs that normally respond to PTH are compromised in one way or the other, thus causing the parathyroid glands to secrete very high quantities of PTH in response to the resulting unresponsively low plasma ionized calcium levels in the blood ( hypocalcemia).

Normal parathyroid glands measure the ionized calcium (Ca) concentration in the blood plasma and secrete parathyroid hormone accordingly: if the ionized calcium rises above normal the secretion of PTH is decreased, whereas when the Ca level falls, parathyroid hormone secretion is increased.

In primary hyperparathyroidism, the release of parathyroid hormone into the blood is no longer determined by the current plasma Ca level, but is persistently above what is appropriate. This may be due to a parathyroid adenoma, which secretes PTH independently of changes in the plasma ionized calcium concentration. This leads to hypercalcemia (abnormally high plasma calcium levels).

Secondary hyperparathyroidism occurs if the plasma ionized calcium level does not respond to changes in PTH secretion from normal glands, and therefore remains abnormally low ( hypocalcemia). The normal glands respond by secreting parathyroid hormone at a persistently high rate. This typically occurs when the 1,25 dihydroxyvitamin D levels in the blood are low or absent. 1,25 Dihydroxyvitamin D (or calcitriol) is the active hormone that determines the quantity of calcium absorbed from the duodenum. Its absence therefore causes hypocalcemia, to which the parathyroid glands respond by secreting large quantities of PTH into the blood (i.e. "secondary hyperparathyroidism"). A lack of 1,25 dihydroxyvitamin D can result from a deficient dietary intake of vitamin D, or from a lack of exposure of the skin to sunlight, so that the body cannot make its own vitamin D from cholesterol. The resulting hypovitaminosis D is usually due to a partial combination of both factors. Vitamin D (or cholecalciferol) is converted to 25-hydroxyvitamin D (or calcidiol) by the liver, from where it is transported via the circulation to the kidneys where it is converted into the active hormone, 1,25 dihydroxyvitamin D. Thus a third cause of secondary hyperparathyroidism is chronic kidney disease. Here the ability to manufacture 1,25 dihydroxyvitamin D is compromised, resulting in hypocalcemia. In both primary and secondary hyperparathyroidism, the high plasma PTH levels erode the skeleton, predisposing it to fractures and bone deformities, necessitating interventions to reverse the high PTH levels in the blood.