PTHafgifte

PTHafgifte refers to the secretion and release of parathyroid hormone (PTH) from the parathyroid glands. PTH is a central regulator of calcium and phosphate homeostasis in humans and many vertebrates. It is stored in secretory granules of the chief cells and released into the bloodstream in response to physiological needs.

The primary trigger for PTHafgifte is the level of ionized calcium in the extracellular fluid. The calcium-sensing receptor (CaSR) on parathyroid cells detects low calcium and stimulates PTH release; higher calcium suppresses secretion. Phosphate levels, magnesium status, and vitamin D status also influence PTH production and release. Chronic changes in these factors can lead to adjustments in PTH gene expression and store depletion.

PTH affects three main targets. In bone, it promotes remodeling by increasing osteoclast activity indirectly through osteoblast signaling (RANKL), releasing calcium and phosphate into the blood. In the kidneys, PTH increases calcium reabsorption in the distal tubule and decreases phosphate reabsorption in the proximal tubule, helping to raise calcium and lower phosphate levels. It also stimulates 1-alpha-hydroxylase, enhancing production of calcitriol (active vitamin D), which increases intestinal absorption of calcium and phosphate. The net result of PTHafgifte is an elevation of serum calcium and a complex regulation of phosphate, with calcitriol production reinforcing intestinal calcium uptake.

Clinically, dysregulation of PTHafgifte occurs in conditions such as primary hyperparathyroidism, secondary hyperparathyroidism (often due to chronic kidney disease or vitamin D deficiency), and hypoparathyroidism. Diagnosis relies on measuring intact PTH alongside calcium and vitamin D status, guiding management to restore calcium-phosphate balance.