PTHrelaterat

PTHrelaterat refers to conditions, mechanisms, and molecules related to parathyroid hormone (PTH) and its related peptide PTHrP. The term commonly appears in medical literature to describe processes that influence calcium and phosphate homeostasis, bone remodeling, development, and certain cancers.

PTH is produced by the chief cells of the parathyroid glands. In response to low serum calcium, PTH raises calcium by promoting bone resorption, increasing renal calcium reabsorption, and stimulating renal production of 1,25-dihydroxyvitamin D, which increases intestinal calcium absorption. It also lowers serum phosphate by promoting its renal excretion.

PTHrP, or parathyroid hormone-related protein, is produced widely in fetal tissues and in various adult tissues. It shares functional similarity with PTH at the PTH1 receptor and is crucial in fetal bone development and placental calcium transport. In oncology, ectopic PTHrP production by tumors can cause humoral hypercalcemia of malignancy, a common cause of non-PTH-mediated hypercalcemia.

Clinically, PTH-related abnormalities include hyperparathyroidism (excess PTH) and hypoparathyroidism (insufficient PTH). Hypercalcemia may arise from excessive PTH or PTHrP activity; distinguishing PTH-mediated from non-PTH-mediated hypercalcemia guides management. Diagnostic workup includes assays of intact PTH, PTHrP, calcium, phosphate, and vitamin D metabolites, along with imaging as indicated.

Treatment depends on the underlying cause: surgical removal of a diseased parathyroid gland in primary hyperparathyroidism; acute management of hypercalcemia with hydration, calcitonin, bisphosphonates, or denosumab; hypoparathyroidism managed with calcium and active vitamin D supplementation; therapy for PTHrP-associated hypercalcemia focuses on treating the tumor and controlling calcium levels.

See also: Parathyroid hormone, PTHrP, hyperparathyroidism, hypoparathyroidism, humoral hypercalcemia of malignancy.