Hyperparathyroidism

Parathyroid hormone (PTH) raises serum calcium. It increases osteoclast-mediated bone resorption, signals the kidneys to retain more calcium, promotes phosphate excretion, and stimulates renal 1-alpha-hydroxylase. The resulting rise in calcitriol, the active form of vitamin D, increases intestinal calcium absorption. This explains an important clinical pattern: excess PTH may produce hypercalcemia, low or low-normal phosphate, increased urinary calcium in some patients, bone loss, and renal stone formation. The hormone is trying to preserve circulating calcium, but chronic exposure shifts calcium out of bone and changes renal handling of phosphate. The effect is not identical in every form of the disorder. Primary disease is usually associated with hypercalcemia. Secondary disease is a compensatory response to a calcium-regulating problem, so calcium may be low or within the reference range. Tertiary disease may become hypercalcemic after the parathyroid glands have been stimulated for years.