PTHsekretionen

PTHsekretionen refers to the release of parathyroid hormone (PTH) from the parathyroid glands. PTH is a peptide hormone produced by the chief cells of the four parathyroid glands and is a central regulator of calcium and phosphate homeostasis. Secretion is tightly governed by the concentration of ionized calcium in the blood via the calcium-sensing receptor (CaSR) on parathyroid cells: low serum calcium stimulates PTH release, while high calcium suppresses it. Magnesium status and phosphate balance can modulate secretion, and calcitriol (active vitamin D) also exerts feedback influences.

PTHacts on bone, kidney, and, indirectly, the intestine. In bone, PTH promotes osteoblasts to increase RANKL expression, which stimulates osteoclast formation and activity, leading to bone resorption and release of calcium and phosphate into the bloodstream. In the kidneys, PTH increases calcium reabsorption in the distal tubule and decreases phosphate reabsorption in the proximal tubule. It also stimulates renal 1α-hydroxylase, raising production of calcitriol, the active form of vitamin D, which enhances intestinal absorption of calcium and phosphate. The net effect is an increase in serum calcium and a decrease in serum phosphate, with calcitriol contributing to longer‑term calcium balance. Rising calcium and calcitriol provide negative feedback to suppress further PTH secretion.

Clinical relevance includes disorders of PTHsekretionen such as primary hyperparathyroidism (autonomous PTH excess), secondary hyperparathyroidism (a response to hypocalcemia, common in chronic kidney disease or vitamin D deficiency), and hypoparathyroidism (reduced PTH due to gland damage or autoimmune causes). PTH measurements support diagnosis and management, and treatment aims to restore calcium homeostasis and bone health.